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Repro-Endo > Hypoglycemia > Flashcards

Hypoglycemia Flashcards

0
Q

Which organ is most dependent on glucose?

A

The brain.

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1
Q

Is hypoglycemia a diagnosis?

A

No it’s a sign. You need to correct the glucose, then determine and correct the underlying problem.

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2
Q

About how long does liver glycogen last in an average fasting adult?

A

24-36 hours

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3
Q

3 sources of glucose?

A

Intake
Glycogenolysis
Gluconeogenesis

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4
Q

4 hormones acting directly on effector organs during fasting?

A

Glucagon
Epinephrine
Cortisol
Growth Hormone

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5
Q

Which processes for fasting adaptation does glucagon increase?

A

Glycogenolysis

Gluconeogenesis

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6
Q

Which processes for fasting adaptation does epinephrine increase?

A

Glycogenolysis
Lipolysis
Ketogenesis

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7
Q

Which process for fasting adaptation does cortisol increase?

A

Gluconeogenesis

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8
Q

Which process for fasting adaptation does growth hormone increase?

A

Lipolysis

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9
Q

Blood glucose cutoffs for…
Activation of counterregulatory processes?
Symptoms of hypoglycemia?
Cognitive dysfunction?

A

Counter-regulation at 65-70mg/dL.
Symptoms at 50-55 mg/dL.
Cognitive dysfunction at 45-50 mg/dL.

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10
Q

Diagnostic and therapeutic thresholds for hypoglycemia?

A

< 50 mg/dL is diagnostic.

< 70 mg/dL merits therapy. (I think that’s what the slide says)

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11
Q

What 3 things compose Whipple’s Triad for hypoglycemia? Why is it important to satisfy them?

A

Symptoms of hypoglycemia.
Measured low blood glucose at time of symptoms.
Correction of symptoms with food/glucose.
Important to satisfy these because the symptoms of hypoglycemia are non-specific.

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12
Q

What are neurogenic vs. neuroglycopenic symptoms of hypoglycemia?

A

Neurogenic: Autonomic (cholinergic and adrenergic) responses to low glucose -palpitations, sweating, hunger, tremor, etc.
Neuroglycopenic: Brain stops working - headache, blurry vision, focal deficients, seizure, etc.

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13
Q

What’s one reason why people can progress to neuroglycopenic symptoms without much warning?

A

Frequent hypoglycemia can blunt the autonomic responses to hypoglycemia - so there’s less warning.
This is called Hypoglycemia-associated Autonomic Failure (HAAF).

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14
Q

Why must you rapidly process blood samples collected for glucose levels?

A

RBCs in there will use it up.

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15
Q

2 clinical types of hypoglycemia?

A

Fasting hypoglycemia: 12-72hrs without food.

Post-prandial hypoglycemia. (uncommon)

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16
Q

4 causes of post-prandial hypoglycemia?

A

Early Dumping Syndrome - in gastric bypass surgery, way food hits gut can cause insulin overreaction.
Early diabetes - dysregulated insulin.
Congenital metabolic disorders - eg. fructose intolerance.
Idiopathic

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17
Q

3 types of fasting hypoglycemia?

A

Insulin-mediated.
Failure of counter-regulation.
Defect in glucose/ketone production.

18
Q

What’s the most common cause of hyperinsulinemic hypoglycemia in adults? In children?

A

Adults: Insulinoma. (I’m surprised it’s not overdose on insulin… maybe that’s not included)
Children: Congenital hyperinsulinism.

19
Q

What happens if you give glucagon in hyperinsulinemic hypoglycemia? How does this contrast with other hypoglycemias?

A

Blood glucose will rise, because liver glycogen is not depleted.
In other hypoglycemias, glycogen is depleted.

20
Q

Review: What do you measure to determine endogenous insulin production?

A

C-peptide.

21
Q

If you have too much insulin, what’s the big picture effect on various energy sources in the blood?

A

There’s no evidence of trying to compensate for low blood sugar:
Glucose low, fatty acids low, ketones low.

22
Q

Proinsulin levels when there’s an insulinoma?

A

Are increased.

23
Q

Treatment for insulinoma?

A

Surgical removal.

24
Q

What’s the most common and severe mutation causing congenital hyperinsulinism? What is the function of this gene/protein normally? Responsiveness to drugs?

A

Loss of function mutations in the ATP-inhibited (that’s my term…) K+ channel of beta calls (SUR or Kir6.2 are the real terms).
Normally, when beta cells are trying to make insulin, ATP is increased, which inhibits this K+ channel, leading to insulin secretion.
This mutation is not diazoxide-responsive.

25
Q

What are the 2 most important drugs used in congenital hyperinsulinism? How do they work?
(there’s a 3rd one mentioned as well…)

A

Diazoxide: Keeps the ATP-inhibited K+ channel of beta cells open.
Somatostatin (analogues): Inhibit Ca++ influx that causes secretory vesicle release.
-Octreotide: Activates ATP-inhibited K+ channel, acts on Ca++ signaling (has more/worse side effects).

26
Q

What do GLUD1 mutations do? Why does that matter?

Treatment for it?

A

Mutations in GLUD1 impair the ability of GTP to inhibit glutamate dehydrogenase (GDH).
Overactive GDH makes too much ATP in beta cells -> inhibition of ATP-inhibited K+ channel -> hyperinsulinemia. (also causes hyperammonemia)
Treatment = diazoxide to keep the K+ channel open.

27
Q

2 different forms of immune-mediated hypoglycemia?

A

Agonist antibodies to insulin receptor.

Anti-insulin antibodies, which can sequester insulin and then release it suddenly in boluses.

28
Q

What are the take-home points about hypoglycemia caused by cortisol and growth hormone deficiencies?

A

It’s more mild, manifests as ketosis during fasting, can be seen by other symptoms/signs of the deficiency, treated with hormone-replacement.

29
Q

3 processes that when disrupted by inborn errors of metabolism can cause hypoglycemia?

A

Glycogenolysis
Gluconeogenesis
Fatty Acid Oxidation / Ketogenesis

30
Q

What processes are messed up by glucose-6-phosphatase deficiency? What remains intact? Treatment?

A

Liver can’t release glucose, so both gluconeogenesis and glycogenolysis are messed up. Ketone production remains intact.
Treatment is for patients to never fast.

31
Q

What happens in Fructose-1,6-diphosphatase deficiency?
What happens during fasting?
Treatment?

A

Can’t “run glycolysis in reverse”-ish for gluconeogenesis.
Fasting -> lactic acidemia. Fructose intolerant.
Treatment is to not fast, avoid fructose.

32
Q

Most common glycogenolysis defect? Treatment? Long term effects?

A

GSD-3 (debrancher)
Treatment: No fasting. Low carb, high protein diet.
Long term complications: Cardiomyopathy and myopathy.

33
Q

Effects of Medium-Chain Acyl-CoA Dehydrogenase deficiency?

A

Impaired ketone production - problems when fasting > 12 hrs.

34
Q

4 common drugs other than insulin that hypoglycemia?

A

Sulfonylurea.
Salicylate overdose (esp in children).
Beta blockers - can produce adrenergic response to hypoglycemia.
Pentamidine (for P. carinii) - destroys beta cells.

35
Q

How can EtOH cause hypoglycemia? What makes this more likely to happen?

A

EtOH metabolism produces lots of NADH, which turns off
gluconeogenesis.
Happens more in children, people on oral glucose-lowering agents, having fasted before EtOH consumption.

36
Q

How can tumors cause hypoglycemia?

A

Lots of different ways… consuming glucose, impairing liver function, impairing nutrition.

37
Q

How can renal disease contribute to hypoglycemia?

A

Loss of protein in urine - less substrate for gluconeogenesis.
Kidney itself does this gluconeogenesis.
Reduced extraction of insulin.

38
Q

3 categories of things to measure when working up hypoglycemia?

A

Counter-regulation - (Insulin, C-peptide, GH, cortisol).
Intermediate metabolites - (beta-hydroxybutyrate, FFAs, lactate, ammonia, etc.).
Other stuff - drug levels.

39
Q

Evaluating hypoglycemia involves…

A

Fasting until glucose < 50mg/dL, taking blood periodically.

Glucagon test.

40
Q

2 things that can cause acidotic, high-lactate hypoglycemia?

A

Gluconeogenic defect.

Alcohol-induced.

41
Q

2 cause of hypoglycemia with acidemia and high ketones?

A

Defect in glycogenolysis.

Defect in counter-regulation.

42
Q

Cause of hypoglycemia without acidemia, with low ketones, high FFAs?

A

Fatty acid oxidation defects (can’t make ketones).

43
Q

Cause of hypoglycemia without acidemia, with low ketones, and low FFAs?

A

Hyperinsulinemia (no signs of trying to compensate for low glucose)

Repro-Endo (60 decks)

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