Hypoglycemia Flashcards

1
Q

When does hypoglycemia occur?

A

Glucose utilization exceeds production

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2
Q

What tissue is absolutely dependent on glucose? What does it use when glucose not available?

A

Brain needs glucose, but uses ketones in absence

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3
Q

What are main tissues of glucose use?

A

Brain, muscle, RBC/WBC, renal medulla

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4
Q

Sources of glucose (3)

A

Ingestion
Gluconeogenesis: long term
Glycogenolysis: exhausted 24-36 hr

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5
Q

Fasting hormonal response on glucose utilization: What are effects of insulin, glucagon, epinephrine, cortisol, growth hormone?

A

Insulin: Suppresses all glucose utilization
Glucagon: Glycogenolysis, gluconeogenesis
Epinephrine: Glycogenolysis, lipolysis, ketogenesis
Cortisol: gluconeogenesis
GH: lipolysis

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6
Q

What happens with decrease in insulin?

A

Increase in fatty acids and ketone generation

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7
Q

At what plasma glucose are symptoms noticeable? Is it above or below levels for hormonal secretion

A

50-55mg/dL

This is below levels for hormonal secretion

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8
Q

Whipple’s Triad

A

Symptoms/signs compatible with hypoglycemia
Low plasma glucose
Resolution of symptoms/signs when plasma glucose restored to normal

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9
Q

Neurogenic symptoms of hypoglycemia: Adrenergic (3) and Cholinergic (3)

A

Result of sympathetic nervous discharge in response to hypoglycemia

Adrenergic: palpitations, tremor, anxiety
Cholinergic: sweating, hunger, paresthesis

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10
Q

Neuroglycopenic Symptoms (big list)

A

Result of failure of brain function
Confusion, dizziness, fatigue, inability to concentrate, blurred vision, headache, focal neurological signs, loss of consciousness, seizures, depressed respiration, death

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11
Q

Which symptoms come first?

A

Neurogenic precede neuroglycopenic symptoms

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12
Q

What is the impact of previous episodes of hypoglycemia? (2)

A

Attenuate adrenergic response

Hypoglycemia-associated autonomic failure

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13
Q

What are 3 broad categories of fasting hypoglycemia?

A
  1. Insulin-mediated (too much insulin) (4)
  2. Failure of counter-regulation (too little counter) (2)
  3. Congenital error of metabolism (3)
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14
Q

What is most common cause (broad) of persistent hypoglycemia? Is the specific cause different for adults vs. children?

A

Most common cause is hyperinsulinemia
For adults most likely due to insulinoma
For children, most likely due to congenital hyperinsulinism

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15
Q

What are diagnostic criteria for hyperinsulinemic hypoglycemia? (5)

A
Hyperinsulinemia
High C-peptide
Hypofattyacidemia 
Hypoketonemia
Glycemic response to glucagon
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16
Q

Are insulinomas big or small? Usually benign or malignant? Where are they located?

A

Typically small and benign.

Usually located in pancreas

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17
Q

What are ectopic locations for insulinomas? (5)

A

Duodenum, Meckel’s diverticulum, bile duct, ovary, omentum

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18
Q

Biochemical profile of insulinomas (3)

A

Elevated insulin, proinsulin (25% of circulating insulin) and C-peptide

19
Q

How are insulinomas treated?

A

Surgical resection

20
Q

What congenital syndrome is associated with congenital hyperinsulinism?

A

Beck with Wiedemann syndrome

21
Q

What is classic presentation of congenital hyperinsulinism? (3)

A

Severe neonatal hypoglycemia
Large birth weight
High glucose requirements

22
Q

Diffuse vs. Focal hyperinsulinism Treatment

A

Focal: remove affected area
Diffuse: need to use therapy

23
Q

Pharmacological Treatment for hyperinsulinemic hypoglycemia: Diazoxide–MOA and AE

A

Activates ATP-dependent K channel

Side effects: fluid retention, hypertrichosis

24
Q

Pharmacological treatment for hyperinsulinemic hypoglycemia: Octreotide–MOA and AE

A

Activates ATP dependent K channel, affects intracellular translocation of Ca, direct inhibition of insulin secretion

Tachyphylaxis, suppression of GH/TSH/ACTH, GI side effects, necrotizing enterocolitis

25
Q

Categories of Autoimmune hypoglycemia

A

Bind to insulin receptor: agonists (hypoglycemia) or antagonists (hyperglycemia)

Insulin antibodies (hirata’s disease): fasting hypoglycemia

26
Q

GH/Cortisol Deficiency: Clues (3)

A

Midline defect, microphallus, cholestatic liver disease

27
Q

GH/Cortisol deficiency: treatment (2)

A

Shorten fasting, hormone replacement

28
Q

Critical samples in GH/cortisol deficiency:

A

Ketone pattern

29
Q

G6Pase deficiency: Clinical (2)

A

Impaired gluconeogenesis/glycogenolysis

Failure to thrive, hepatomegaly

30
Q

G6Pase deficiency: Labs (3) and test (1)

A

Hyperlacticacidemia, hyptertriglyceridemia, hyperuricemia

Lack of glycemic response to fed glucagon stimulation test

31
Q

G6Pase deficiency: Treatment (4)

A

Frequent carb-rich meals
Intragastric dextrose
Uncooked cornstarch
No lactose/fructose

32
Q

G6Pase deficiency: Types

A

Glycogen storage disease 1a

Glycogen storage 1b (10%): added neutropenia

33
Q

F1,6BP deficiency: Clinical signs and trigger

A

Attacks of acidemia, hyperlacticacidemia, hyperuricemia

Triggered by fasting/fructose

34
Q

F1,6BP deficiency: Rx (2)

A

Limit fasting to less than 8-12 hours

No fructose/sucrose

35
Q

Glycogen Debrancher Deficiency (GSD type 3): Clinical signs (3)

A

Failure to thrive, hepatomegaly, muscle weakness

36
Q

Glycogen Debrancher Deficiency (GSD type 3): labs

A

Impaired glycogenolysis: hyperketonemia

37
Q

Glycogen Debrancher Deficiency (GSD type 3): Rx (3)

A

Frequent low carb feeds
Intragastric dextrose
Uncooked cornstarch

38
Q

Late symptoms of Glycogen Debrancher Deficiency (GSD type 3) (2)

A

Cardiomyopathy

Myopathy

39
Q

Medium Chain Acyl-CoA Dehydrogenase Deficiency–FAO defect: Signs (2)

A

Hypoketotic hypoglycemia

Mimics Reye’s syndrome

40
Q

Medium Chain Acyl-CoA Dehydrogenase Deficiency–FAO defect: Rx (1)

A

Limit fasting to less than 12 hours

41
Q

Hypoglycemia due to drugs (4)

A

Sulfonylureas
Salicylate OD
Beta-adrenergic blocking agents (no adrenergic warning signs, HHS pattern)
Pentamidine for pneumocystis

42
Q

What substance can stimulate hypoglycemia in fasting state? How does it do this?

A

Alcohol; by using NDH

43
Q

DDX of Hypoglycemia based on critical sample

A

See chart! Know chart!