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Endocrine > Hypoglycemia > Flashcards

Hypoglycemia Flashcards

1
Q

T/F Hypoglycemia is a diagnosis

A

F –> sign

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2
Q

Stored glycogen is depleted in the adult after _____ hours of fasting

A

24-36

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3
Q

In the first few hours of fasting, the main source of glucose comes from ____

A

glycogenolysis (and a little bit of gluconeogenesis)

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4
Q

Does the quantity of the hormone increase or decrease during fasting? GH

A

Growth hormone increases

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5
Q

Does the quantity of the hormone increase or decrease during fasting? ACTH

A

increases

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6
Q

Does the quantity of the hormone increase or decrease during fasting? cortisol

A

increases

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7
Q

Does the quantity of the hormone increase or decrease during fasting? Epinephrine

A

increases

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8
Q

Does the quantity of the hormone increase or decrease during fasting? Insulin

A

decreases

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9
Q

Does the quantity of the hormone increase or decrease during fasting? glucagon

A

increases

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10
Q

Which 2 hormones upregulate glycogenolysis?

A

glucagon and epinephrine

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11
Q

Which 2 hormones upregulate gluconeogenesis?

A

glucagon and cortisol

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12
Q

Which 2 hormones upregulate lipolysis?

A

epinephrine and growth hormone

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13
Q

Which hormone upregulates ketogenesis?

A

epinephrine

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14
Q

Decrease in insulin is accompanied by increase/decrease in free fatty acids and ketone bodies.

A

increase

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15
Q

Ketone bodies (2)

A

beta hydroxybutyrate and acetoacetate

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16
Q

What is therapeutic hypoglycemia?

A

the point at which body starts responding to low glucose –> 65-70 mg/dL

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17
Q

What is diagnostic hypoglycemia?

A

the point at which symptoms of hypoglycemia reveal themselves –> 50-55 mg/dL

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18
Q

At what glucose level does cognitive dysfunction begin?

A

45-50 mg/dL

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19
Q

Whipple’s Triad

A

Required for diagnosis of hypoglycemia: symptoms of hypoglycemia, measured low glucose at time of symptoms, correction of symptoms with food or glucose

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20
Q

Neurogenic symptoms of hypoglycemia

A

CNS sympathetic discharge –> adrenergic (palpitations, tremor, anxiety) and cholinergic (sweating, hunger,paresthesis)

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21
Q

Neuroglycopenic symptoms of hypoglycemia

A

confusion, dizziness, fatigue, concentration, vision, headache, focal signs, seizures, etc.

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22
Q

What comes first, neurogenic or neuroglycopenic symptoms?

A

neurogenic

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23
Q

HAAF

A

hypoglycemia associated autonomic failure: previous episodes of hypoglycemia may reduce response to later episodes

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24
Q

T1d may often lose glucagon producing islet cells and may lose ____ response as well making them vulnerable to hypoglycemia

A

epinephrine

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25
Q

T/F glucose levels fall in collection tubes not containing glycolysis inhibitors

A

T –> used by red and white cells –> glucose meters are not accurate –> need rapid processing of plasma glucose

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26
Q

Hypoglycemia occurring 12-72 hours after food deprivation

A

fasting hypoglycemia

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27
Q

Hypoglycemia occurring in reaction to food consumption and not while fasting

A

post prandial hypoglycemia –> uncommon

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28
Q

Causes of post-prandial hypoglycemia

A

late dumping syndrome (after gastric surgery), early diabetes, reactive hypoglycemia/idiopathic, congenital metabolic disorders

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29
Q

Causes of fasting hypoglycemia

A

hyerpinsulinism, insulinomas, autoimmune hypoglycemia, growth hormone deficiency, cortisol deficiency, congenitally impaired glycogenolysis, gluconeogenesis, and ketogenesis

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30
Q

Most common cause of persistent hypoglycemia in children/adults

A

insulinomas in adults and congenital hyperinsulinism in children

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31
Q

Dx criteria for hyperinsulinemic hypoglycemia

A

increased glucose utilization –> hyperinsulinemia, high cpeptide, hypofattyacidemia,hypoketonemia, glycemic response to glucagon –> during hypoglycemia

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32
Q

Insulinoma

A

typically small, benign (90%), solitary, located in pancreas

33
Q

Tx of insulinoma

A

surgical resection

34
Q

GDH

A

glutamate dehydrogenase –> breaks down glutamate formed from amino acids –> increases ATP –> K+ channel –> calcium release –> insulin release form beta cells

35
Q

Somatostatin MOA

A

inhibit insulin release by affecting calcium and potassium channels in beta cells

36
Q

Glucokinase mutation in hyperinsulinism

A

dominant gain of function –> lowers glucose threshold for insulin release

37
Q

GDH mutation in hyperinsulinism

A

dominant gain of function of GLUD1 –> impair GTP inhibition of GDH –> lowers protein threshold for insulin release

38
Q

K+ channel mutation in hyperinsulinism

A

rec/dominant loss of function of K+atp channel

39
Q

HNF4A and HNF1A

A

dominant mutations in transcription factors that present as hypoglycemia early on and then progress to diabetes later in life

40
Q

Most common and severe form of congenital hyperinsulinism

A

Katp –> mutations of SUR1 or Kir6.2

41
Q

T/F Katp hyperinsulinism is unresponsive to diazoxide

A

T

42
Q

T/F Katp hyperinsulinism may be focal or diffuse

A

T

43
Q

Classical features of GDH hyperinsulinemia

A

fasting/post prandial hypoglycemia + hyperammonemia (GLUD1 is also in kidney)

44
Q

T/F GDH hyperinsulinemia is diazoxide responsive

A

T

45
Q

Side effects of diazoxide

A

fluid retention, hypertichosis

46
Q

Octreotide MOA

A

activates Katp channel, affects intracellular translocation of Ca, direct inhibition of insulin secretion

47
Q

Side effects of octreotide

A

suppression of GH, TSH, ACTH, GI side effects, necrotizing entercolitis

48
Q

Immune mediated hypoglycemia

A

antibodies to insulin receptor –> act as insulin agonist or against insulin itself to cause hypoglycemia (or antagonist to cause hyperglycemia) –> self limited and tx usually unsuccessful

49
Q

GH/Cortisol deficiency-mediated hypoglycemia

A

shorten fasting (partial impairment of gluconeogenx and lipolysis)

50
Q

Tx of GH/Cortisol deficiency-mediated hypoglycemia

A

replacement of deficient hormones

51
Q

Clinical clues of GH/Cortisol deficiency-mediated hypoglycemia

A

midline defect, microphallus, cholestatic liver disease

52
Q

G6PD

A

converts G6P to glucose –> hypoglycemia if G6PD –> complete dependence on exogenous glucose –> failure to thrive, hepatomegaly

53
Q

Lab features of G6PD

A

hyperlacticacidemia, hypertriglyceridemia, hyperuricemia, lack of glycemic response to fed glucagon stim test

54
Q

Two types of G6PD

A

GSD 1a (90%) and 1b

55
Q

Tx of G6PD

A

constant feeding

56
Q

How do G6PD patients survive during fasting

A

production of ketones

57
Q

F16PD

A

converts F16P–>F6P…glucose –> attacks of acidemia, hyperuricemia, hyperlacticacidemia

58
Q

T/F glycogenolysis is intact in F16PD

A

T –> longer fasting tolerance than G6PD

59
Q

T/F gluconeogenesis is intact in F16PD

A

F –> hypoglycemia with fasting or with fructose consumption (can’t convert it)

60
Q

Tx of F16PD

A

limit fasting and no fructose/sucrose

61
Q

Debrancher deficiency/GSD type 3

A

can’t break down glycogen –> failure to thrive, hepatomegaly, weakness of muscle

62
Q

Key feature of debrancher deficiency

A

hyperketonemia and elevated AST/ALT

63
Q

Tx of debrancher deficiency

A

frequent low CHO feeds

64
Q

T/F cardiomyopathy is not a late consequence of debrancher deficiency

A

F

65
Q

MCAD deficiency

A

cannot break down acyl-coA chains –> hypoketotic hypoglycemia

66
Q

key feature of MCAD deficiency

A

elevated LFT/NH3

67
Q

Tx of MCAD deficiency

A

limit fasting

68
Q

Screening for MCAD deficiency

A

newborn screening by MS acyl-carnitine

69
Q

Drugs causing hypoglycemia

A

sulfonylurea, salicylate overdose, beta adrenergic blockers, pentamidine (pneumocystis)

70
Q

MOA beta adrenergic blocking agents and hypoglycemia

A

impaired lipolysis –> hypoketotic hypoglycemia

71
Q

Alcohol induced hypoglycemia

A

oxidation of ethanol –> NADH –> inhibition of enzymes in gluconeogenesis –>only occurs if hepatic glycogen stores are depleted

72
Q

Non-islet cell tumors

A

mesenchymal (retroperitoneal/thoracic sarcomas, fibromas, mesotheliomas, hemangiopericytomas), epithelial (hepatoma, renal cell carcinoma, nonislet cell tumor of pancreas, carcinoid), leukemia/lymphoma

73
Q

etiology of tumor hypoglycemia

A

poor nutrition with advanced malignancy, tumor consumption of glucose, reduced hepatic gluconeogenesis/tumor production of insulin like factors, metastatic disease of liver

74
Q

T/F sepsis can cause hypoglycemia

A

T

75
Q

Diff Dx: hypoglycemia with acidemia and high lactate

A

gluconeogenic defect, alcohol induced

76
Q

Diff Dx: hypoglycemia with acidemia and low lactate

A

glycogenolysis or counterregulation defect

77
Q

Diff Dx: hypoglycemia with high fatty acids

A

FAO defect

78
Q

Diff Dx: hypoglycemia with low FFA, low ketones, no acidemia

A

hyperinsulinemic hypoglycemia

79
Q

Key feature of insulin-mediate hypoglycemia

A

suppressed ketones

Endocrine (26 decks)

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