Endocrine/Electrolyte Flashcards

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1
Q

DKA and HHS represent a spectrum of complications from DM and differ mainly in what 3 ways?

A

Level of hyperglycemia
Extent of dehydration
Presence and degree of ketoacidosis

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2
Q

Contrast the populations presenting with DKA vs. HHS.

A

DKA: younger patients (<65 y/o) with DM1, usually evolves rapidly over 24 hours

HHS: older patients (>65 y/o) with DM2, evolves over several days

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3
Q

Define hyperglycemia.

A

Fasting (8 hrs): >90-130 mg/dL

Postprandial >180 mg/dL

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4
Q

Describe DKA and its common causes.

A

Absolute insulin deficiency, hyperglycemia, AG acidosis, dehydration

Infection, disruption of insulin therapy, presentation of new onset DM

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5
Q

Describe HHS and its common causes.

A

Hyperglycemia
Hyperosmolarity
Dehydration
WITHOUT significant ketoacidosis

Poorly controlled DM2 with underlying infection

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6
Q

Which has a higher mortality rate - HHS or DKA?

A

HHS

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7
Q

Initial actions/primary survey in hyperglycemia/HHS/DKA?

A

Mild to moderate hyperglycemia/minor symptoms - anticipatory guidance and proper follow-up

BG>300-350: UA (ketones?), then BMP to exclude AG acidosis, +/- IVF

Ill-appearing, hemodynamically unstable/DKA/HHS - ABCs, 2 large bore IVs, normal saline 1-2L (adult), bolus 20 cc/kg (child), monitor

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8
Q

What conditions can affect diabetic patients resulting in an increase in counter-regulatory hormones and hyperglycemia and precipitate DKA/HHS?

A
Cocaine use
Infection/sepsis
MI
Surgery
Trauma
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9
Q

Classic presentation of hyperglycemia?

A

Mild - asymptomatic
BG>180 mg/dL - osmotic diuresis; polyuria, polydipsia, polyphagia, weight loss
Some will have tachycardia, dizziness, lightheadedness, and weakness as a result of dehydration/lyte imbalance

Progression - abdominal pain, hyperpneic respirations (fast and deep Kaussmaul respirations), hypotension, ketotic breath, marked tachycardia, neuro symptoms (HHS)

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10
Q

Lab tests for hyperglycemia/DKA/HHS?

A
POC glucose
UA
BMP
CBC
VBG
Phos, Mag
EKG
Additional testing based on patient presentation (lipase, hepatic functions, CXR, BCx, etc.)
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11
Q

Lab findings in DKA?

A
Glucose: >250
Arterial pH: <7.3
Serum bicarb: <18
Urine ketones: +++
Serum ketones: +++
Serum Osm: increased
AG: >>>12
Mental status: variable
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12
Q

Lab findings in HHS?

A
Glucose: >600
Arterial pH: >7.3
Serum bicarb: >18
Urine ketones: -/faintly +
Serum ketones: -/faintly +
Serum Osm: very increased
AG: Normal (12-16)
Mental status: stupor/coma
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13
Q

Rx uncomplicated mild to moderate hyperglycemia?

A

IV fluids

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14
Q

Rx DKA and HHS?

A

Fluid replacement
Management of electrolyte abnormalities
Insulin replacement therapy
ID underlying precipitants

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15
Q

How is fluid replacement done in DKA/HHS?

A

Avg loss in DKA 3-6 L, HHS 8-10 L
Start with NS at 15-20 mL/kg/hr for the first few hours
Switch to 0.45% saline when the serum sodium normalizes
Add dextrose to IV fluids when serum glucose reaches 250 mg/dL

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16
Q

Insulin replacement in DKA/HHS?

A

Start only after adequate fluid resuscitation
Start with an infusion of regular insulin at 0.1 U/kg/hr
Double the dose of insulin if the blood glucose does not fall by 50-70 mg/dL in the first hour

17
Q

Potassium replacement in DKA/HHS?

A

If initial K <3.3 mEq/L then DELAY insulin therapy until fluid and K replacement

Give K with initial fluid replacement if K levels are normal or low and maintain between 4-5

18
Q

Use of bicarb in DKA/HHS?

A

Controversial, as it may cause a paradoxical fall in cerebral pH and neuro deterioration

Certain situations may warrant use:
Severe acidosis with pH <6.9
Severe life-threatening hyperkalemia
Seizures
Cardiac or persistently hypotensive patient
19
Q

Serial monitoring in DKA/HHS?

A

BG every hour until stable, then every 2-4 hours

BMP and blood pH Q2-4 hours during therapy until stabilized