Acute Complications of Diabetes Flashcards

1
Q

3 main acute complications of diabetes

A

Diabetic ketoacidosis
Hyperglycemic hyperosmolar syndrome
Hypoglycemia

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2
Q

Diabetic ketoacidosis (what is it, and what 4 things is it characterized by)

A

Metabolic decompensation resulting from an absolute (or close to) insulin deficiency
Usually in T1D
Characterized by: hyperglycemia, metabolic acidosis, ketones in blood, volume depletion

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3
Q

Clinical features of DKA

A
Prodrome (1-2 days of polydypsia/uria (from hyperglycemia), weakness, nausea, vomiting, abdo pain)
Volume depletion
Tachypnea
Acetone (fruity) breath
Myalgia (from anaerobic metabolism)
Normal temp or hypothermia (bad sign)
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4
Q

Kussmaul breathing

A

Rapid deep inspirations

Trying to compensate for metabolic acidosis

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5
Q

4 precipitating conditions for DKA

A

Acute illness (infection, stroke, MI, pancreatitis)
New onset diabetes
Insulin under-dosing
Drugs (alcohol, cocaine, lithium)

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6
Q

Mechanism of DKA

A

Absolute insulin deficiency
Loss of glucagon suppression
Excess glucagon results in increased gluconeogenesis and ketogenesis

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7
Q

Triad of DKA

A

Hyperglycemia
Metabolic acidosis
Ketosis

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8
Q

Anion gap

A
Positive ions (Na) - negative ions (Cl and bicarb)
Normal is 10-14
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9
Q

How is the anion gap affected in DKA?

A

Wider! More than 16

Because you have less bicarb (buffering the acid)

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10
Q

3 things we want to treat first in DKA

A

Volume
Hyperkalemia
Ketogenesis

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11
Q

Management of DKA

A
Volume repletion with normal saline
Stop ketogenesis (give insulin)
K repletion (slowly)
Normalize glucose
Treat precipitating condition
Avoid complications
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12
Q

What is the biggest risk complication of pediatric DKA?

A

Cerebral edema

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13
Q

Cushing’s triad

A

A sign of increased intracranial pressure

Hypertension, bradycardia, irregular respiration

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14
Q

Management of suspected cerebral edema

A

Don’t wait!!
Elevate the head, reduce IV fluids
Give mannitol (osmotically active - decreases blood viscosity and improves cerebral blood flow)
Give 3% hypertonic saline (instead of or along with mannitol - lowers ICP, increases intravascular volume and MAP)

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15
Q

Hyperglycemic hyperosmolar state (what is it, what is it characterized by)

A

Metabolic decompensation resulting from relative insulin deficiency and severe hyperglycemia and volume depletion
Usually T2D
Characterized by: hyperosmolality, hyperglycemia, volume depletion

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16
Q

Clinical features of HHS

A
Often elderly
Prodrome (polydipsia/uria, weakness, confusion, lethargy)
Poor fluid intake
Volume depletion
Hypothermia
17
Q

Precipitating conditions of HHS

A
Acute illness (infection, MI, stroke, pancreatitis, PE, bowel obstruction, renal failure, subdural hematoma, burns, heat stroke)
Drugs (Ca channel blockers, phenytoin, thiazides)
18
Q

Normal plasma osmolality value

A

285-295 mosm/L

19
Q

Management of HHS

A
Volume repletion (1/2 saline)
Normalize glucose (insulin)
K repletion
Treat precipitating condition
Monitor
20
Q

pH and glucose in DKA and HHS

A

DKA: severe acidosis, moderate hyperglycemia
HHS: mild acidosis/normal pH, severe hyperglycemia
Normal is pH 7.25 to 7.30

21
Q

Clinical features of hypoglycemia

A

Autonomic (E/NE): sweating, tachycardia, tremor, hunger, anxiety, warm, nausea
Neuroglycopenic (CNS): dizzy, weak, blurred vision, drowsiness, confusion, seizure/coma

22
Q

Risk factors for hypoglycemia

A
Elderly, cognitive dysfunction/dementia
Liver/kidney dysfunction
Adrenal insufficiency
Lack of diabetes education
Alcohol consumption
Exercise
Food insecurity, missed/delayed meals
Certain medications
23
Q

Treatment of hypoglycemia

A

Home glucagon injection kits
Strict avoidance of hypoglycemia
Rapid acting glucose