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Endorine > Hypoglycemia > Flashcards

Hypoglycemia Flashcards

1
Q

What is hypoglycemia

A

A sign, not a diagnosis. Results when glucose utilization exceeds production

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2
Q

What are the main tissues of glucose use?

A

Muscle, red and white cells, renal medulla

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3
Q

What are the sources of glucose?

A

Ingestion, glycogenolysis, gluconeogenesis

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4
Q

How long until glycogen stores are depleted in adult?

A

After 24-36 hrs of fasting

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5
Q

Where does gluconeogenesis occur?

A

Liver, renal cortex, from lactate, glycerol and amino acids (alanine in liver, glutamine in renal cortex)

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6
Q

What 3 systems must fail to result in hypoglycemia?

A

Glycogenolysis, gluconeogenesis, ketogenesis

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7
Q

Hormonal control of insulin

A

Stops glycogenolysis, gluconeogenesis, lipolysis, ketogenesis

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8
Q

Hormonal control of glucagon

A

Promotes glycogenolysis, gluconeogenesis

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9
Q

Hormonal control of epinephrine

A

Promotes glycogenolysis, lipolysis and ketogenesis

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10
Q

Hormonal control of cortisol

A

Promotes gluconeogenesis

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11
Q

Hormonal control of growth hormone

A

Promotes lipolysis

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12
Q

What range of glucose is normal

A

60-100mg/dL

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13
Q

What is a dec in insulin accompanied by

A

-inc in free FAs and ketone body generation (beta hydroxybutyrate and acetoacetate)

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14
Q

How much glucose should be in the blood to suppress insulin secretion

A

80-85mg/dL

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15
Q

How much glucose should be in the blood to increase glucagon release

A

65-70mg/dL

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16
Q

How much glucose should be in the blood to increase epinephrine release

A

65-70mg/dL

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17
Q

How much glucose should be in the blood to increase cortisol and growth hormone

A

65-70mg/dL

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18
Q

How much glucose should be in the blood to be aware of symptoms

A

50-55mg/dL

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19
Q

How much glucose should be in the blood to impair cognition

A

<50mg/dL

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20
Q

What is Whipple’s triad?

A

Must be satisfied to be hypoglycemia

  1. Symp and/or signs compatible with hypoglycemia
  2. A low measured plasma glucose concentration
  3. Resolution of symptoms/signs when glucose concentration is normalized

Symptoms are characteristics, but non-specific

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21
Q

What 2 broad categories of symptoms of hypoglycemia?

A

Neurogenic and neuroglycopenic

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22
Q

What are the neurologic symptoms of hypoglycemia?

A

Neurogenic (autonomic): adrenergic (palpitations, tremor, anxiety) and cholinergic (sweating, hunger, paresthesis)

Sympathetic nervous discharged is triggered by hypoglycemia: how the pts become aware of it

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23
Q

What are the neuroglycopenic symptoms of hypoglycemia?

A

Arise from failure of brain fxn caused by deficient glucose: confusion. dizziness, fatigue, inability to concentrate, blurred vision, headache, focal neurological signs, loss of consciousness, seizures, depression of respiration, death

24
Q

Which symptoms come first?

A

NEurogenic precede neuroglycopenic

25
Q

What is HAAF?

A

Hypoglycemia associated autonomic failure: hypoglycemia unawareness because prev episodes of hypoglycemia may modify response to a later episode, typically attenuating the adrenergic response

26
Q

What happens to T1D alpha cells?

A

T1D pts often lose glucagon-producing islet cells and may lose epinephrine response as well, making them vulnerable to hypoglycemia

27
Q

What is fasting hypoglycemia?

A

Occurs 12-72 hours after food deprivation (shorter in individuals with excessive insulin)–>most cases

28
Q

What is post prandial hypoglycemia/reactive

A

Occurs in reaction to food consumption and not while fasting–>very uncommon

29
Q

What are some examples of post-prandial hypoglycemia?

A
  • Late dumping syndrome
  • Early diabetes
  • REactive
  • Certain congenital metabolic disorders (galactosemia, hereditary fructose intolerance)
30
Q

What are possible causes of fasting hypoglycemia?

A

Insulin mediated
Failure of counter regulation
Convenital metabolic disorders

31
Q

What is the most common cause of persistent hypoglycemia?

A

Hyperinsulinemic hypoglycemia

32
Q

What is the most common cause of persistent hypoglycemia in adults?

A

Insulinomas

33
Q

What is the most common cause of persistent hypoglycemia in children?

A

congeintal hyperinsulinism

34
Q

What is hyperinsulinemic hypoglycemia?

A

Caused by increased glucose utilization in the presence of too much insulin

35
Q

Diagnostic criteria for hyperinsulinemic hypoglycemia?

A
  • During the hypoglycemic state, labs will also show: hyperinsulinemia, high C-peptide, dec free fatty acids, hypoketonemia, and a glycemic response to injected glucagon (this is important to know) -> the high insulin suppresses glycogenolysis, so glucagon will induce utilization of stored glycogen
  • inc glucose utilization
36
Q

Treatment of hyperinsulinemic hypoglycemia?

A

Treatment: diazoxide, which activates the KATP channel to close, and octreotide, which affects intracellular Ca2+, inhibiting insulin secretion.

37
Q

What are insulinomas?

A

Most common cause of endogenous hyperinsulinemia in adults. They are benign in over 90% of cases, usually located within the pancreas, and treated with surgery.

38
Q

What is the diagnosis of insulinomas?

A

During the hypoglycemic state, labs will also show: elevated insulin, elevated C-peptide, and elevated proinsulin -> the tumor cells don’t process proinsulin properly, so the ratio of circulating insulin to proinsulin will be abnormal

39
Q

Treatment of insulinomas?

A

Surgical resection

40
Q

What is congenital hyperinsulinism?

A

Most common cause of hyperinsulinemia in kids. There are multiple known mutations that result in increased insulin production/release.

41
Q

What is the normal process that leads to insulin release?

A

Glucose enters the pancreatic beta cell and is converted to ATP in a pathway involving the glucokinase enzyme. ATP stimulates a K+ channel to close, which depolarizes the beta cell, opening a voltage-dependent Ca2+ channel. The influx of Ca2+ triggers insulin release. Also, the beta cell can convert amino acids (leucine, glutamate) into ATP, using the GDH enzyme, which then follows the same pathway.

42
Q

Katp Channel Mutation

A

Loss of function leads to dysregulated insulin release. Can be diffuse throughout the entire pancreas or affect only a fraction of beta cells.

Signs: severe hyperinsulinemia, neonatal onset, large gestational age

Diazoxide unresponsive. This is a drug that targets the K+ channel, stimulating it to remain open. The mutated KATP channel is unaffected by this therapy.

Most common and severe form of congenital HI

43
Q

GDH-HI (hyperinsulinism/hyperammonemia syndrome)

A

GDH mutation: leads to the loss of GDH inhibition, meaning the enzyme is always on, creating too much ATP within the beta cell. (activating mutation)

Co-presents with hyperammonemia (enzyme also plays a role in ammonia clearance in kidneys)

Signs: mild, late onset, normal birth weight

Diazoxide responsive

44
Q

Autoimmune hypoglycemia

A

Autoimmune: (rare) can be caused by antibodies to the insulin receptor, which act as either agonists (resulting in hypoglycemia) or antagonists (causing hyperglycemia).

Antibodies to insulin can also be present (Hirata’s disease), which trap insulin in circulation and then release it at random

Disease is usually self-limited

Treatment: immunosuppression, steroids, plasmapheresis generally unsuccessful

45
Q

Growth hormone/cortisol deficiency

A

Failure of counter regulation

Partial impairment of gluconeogenesis and lipolysis, leading to decreased tolerance of fasting.

Will present with hypoglycemia and elevated ketones

Treatment: replace deficient hormones

46
Q

G6P Deficiency

A

Congenital metabolic disorder (inborn error of metab)

G6P is necessary to release synthesized glucose from the liver (either from glycogenolysis or ketogenesis). Patients w/ this deficiency can only utilize glucose that they take in from meals, so this is treated with frequent feeding.

Labs: high triglycerides, lactic acid, uric acid, and a lack of glycemic response to a glucagon stimulation test

2 mutations: GSD 1a (90%) and 1b. People with 1b can get neutropenia making them more susceptible to infections

Can’t eat lactose/fructose

47
Q

Fructose-1,6-P deficiency

A

Prevents production of glucose from lactate in the liver

Get attacks of acidemia, hyperlacticacidemia, hyperuricemia

Triggers: fasting or fructose

Treatment: limit fasting <8-12hrs, no fructose/sucrose

48
Q

Glycogen debrancher deficiency

A

Results in accumulation of glycogen in liver and muscle and may lead to liver failure

Clinical: failure to thrive, hepatomegaly, muscle weakness

Labs: hyperketonemia, inc liver enzymes

Can lead to cardiomyopathy and myopathy because can’t break down glycogen

49
Q

MCAD Deficiency

A

Medium-Chain Acyl-CoA Dehydrogenase Definiency

  • Hypoketotic hypoglycemia
  • Screen in new borns
  • Limit fasting <12 hrs
50
Q

What drugs cause hypoglycemia?

A

Sulfonylureas
Salicylate OD
Beta adrenergic blocking agents
-Pentamidine

51
Q

Alcohol induced hypoglycemia

A

Common in T1D, oxidation of ethanol to acetic acid generates NADH, which can inhibit several gluconeogenic enzymes including conversion of lactate and AAs to pyruvate

Presents with hypoglycemia ~6-36 hours after eating

52
Q

Non-islet cell tumors

A

Present sign or herald recurrence of tumor

Mesenchymal, epithelial or leukemia and lymphoma

53
Q

Etiology of tumor hypoglycemia

A

Poor nutrition with advanced malignancy, tumor consumes glucose, reduced hepatic gluconeogenesis, metastatic disease involving the liver

54
Q

Hepatic and renal disease

A

Can disrupt gluconeogenesis or cause substrate deprivation (like muscle wasting due to renal dis)

55
Q

Sepsis

A

Can also cause hypoglycemia

56
Q

SEE END OF SLIDES–starting at EVAL

A

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Endorine (24 decks)

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