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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
T/F glucose levels fall in collection tubes not containing glycolysis inhibitors
T --> used by red and white cells --> glucose meters are not accurate --> need rapid processing of plasma glucose
26
Hypoglycemia occurring 12-72 hours after food deprivation
fasting hypoglycemia
27
Hypoglycemia occurring in reaction to food consumption and not while fasting
post prandial hypoglycemia --> uncommon
28
Causes of post-prandial hypoglycemia
late dumping syndrome (after gastric surgery), early diabetes, reactive hypoglycemia/idiopathic, congenital metabolic disorders
29
Causes of fasting hypoglycemia
hyerpinsulinism, insulinomas, autoimmune hypoglycemia, growth hormone deficiency, cortisol deficiency, congenitally impaired glycogenolysis, gluconeogenesis, and ketogenesis
30
Most common cause of persistent hypoglycemia in children/adults
insulinomas in adults and congenital hyperinsulinism in children
31
Dx criteria for hyperinsulinemic hypoglycemia
increased glucose utilization --> hyperinsulinemia, high cpeptide, hypofattyacidemia,hypoketonemia, glycemic response to glucagon --> during hypoglycemia
32
Insulinoma
typically small, benign (90%), solitary, located in pancreas
33
Tx of insulinoma
surgical resection
34
GDH
glutamate dehydrogenase --> breaks down glutamate formed from amino acids --> increases ATP --> K+ channel --> calcium release --> insulin release form beta cells
35
Somatostatin MOA
inhibit insulin release by affecting calcium and potassium channels in beta cells
36
Glucokinase mutation in hyperinsulinism
dominant gain of function --> lowers glucose threshold for insulin release
37
GDH mutation in hyperinsulinism
dominant gain of function of GLUD1 --> impair GTP inhibition of GDH --> lowers protein threshold for insulin release
38
K+ channel mutation in hyperinsulinism
rec/dominant loss of function of K+atp channel
39
HNF4A and HNF1A
dominant mutations in transcription factors that present as hypoglycemia early on and then progress to diabetes later in life
40
Most common and severe form of congenital hyperinsulinism
Katp --> mutations of SUR1 or Kir6.2
41
T/F Katp hyperinsulinism is unresponsive to diazoxide
T
42
T/F Katp hyperinsulinism may be focal or diffuse
T
43
Classical features of GDH hyperinsulinemia
fasting/post prandial hypoglycemia + hyperammonemia (GLUD1 is also in kidney)
44
T/F GDH hyperinsulinemia is diazoxide responsive
T
45
Side effects of diazoxide
fluid retention, hypertichosis
46
Octreotide MOA
activates Katp channel, affects intracellular translocation of Ca, direct inhibition of insulin secretion
47
Side effects of octreotide
suppression of GH, TSH, ACTH, GI side effects, necrotizing entercolitis
48
Immune mediated hypoglycemia
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
GH/Cortisol deficiency-mediated hypoglycemia
shorten fasting (partial impairment of gluconeogenx and lipolysis)
50
Tx of GH/Cortisol deficiency-mediated hypoglycemia
replacement of deficient hormones
51
Clinical clues of GH/Cortisol deficiency-mediated hypoglycemia
midline defect, microphallus, cholestatic liver disease
52
G6PD
converts G6P to glucose --> hypoglycemia if G6PD --> complete dependence on exogenous glucose --> failure to thrive, hepatomegaly
53
Lab features of G6PD
hyperlacticacidemia, hypertriglyceridemia, hyperuricemia, lack of glycemic response to fed glucagon stim test
54
Two types of G6PD
GSD 1a (90%) and 1b
55
Tx of G6PD
constant feeding
56
How do G6PD patients survive during fasting
production of ketones
57
F16PD
converts F16P-->F6P...glucose --> attacks of acidemia, hyperuricemia, hyperlacticacidemia
58
T/F glycogenolysis is intact in F16PD
T --> longer fasting tolerance than G6PD
59
T/F gluconeogenesis is intact in F16PD
F --> hypoglycemia with fasting or with fructose consumption (can't convert it)
60
Tx of F16PD
limit fasting and no fructose/sucrose
61
Debrancher deficiency/GSD type 3
can't break down glycogen --> failure to thrive, hepatomegaly, weakness of muscle
62
Key feature of debrancher deficiency
hyperketonemia and elevated AST/ALT
63
Tx of debrancher deficiency
frequent low CHO feeds
64
T/F cardiomyopathy is not a late consequence of debrancher deficiency
F
65
MCAD deficiency
cannot break down acyl-coA chains --> hypoketotic hypoglycemia
66
key feature of MCAD deficiency
elevated LFT/NH3
67
Tx of MCAD deficiency
limit fasting
68
Screening for MCAD deficiency
newborn screening by MS acyl-carnitine
69
Drugs causing hypoglycemia
sulfonylurea, salicylate overdose, beta adrenergic blockers, pentamidine (pneumocystis)
70
MOA beta adrenergic blocking agents and hypoglycemia
impaired lipolysis --> hypoketotic hypoglycemia
71
Alcohol induced hypoglycemia
oxidation of ethanol --> NADH --> inhibition of enzymes in gluconeogenesis -->only occurs if hepatic glycogen stores are depleted
72
Non-islet cell tumors
mesenchymal (retroperitoneal/thoracic sarcomas, fibromas, mesotheliomas, hemangiopericytomas), epithelial (hepatoma, renal cell carcinoma, nonislet cell tumor of pancreas, carcinoid), leukemia/lymphoma
73
etiology of tumor hypoglycemia
poor nutrition with advanced malignancy, tumor consumption of glucose, reduced hepatic gluconeogenesis/tumor production of insulin like factors, metastatic disease of liver
74
T/F sepsis can cause hypoglycemia
T
75
Diff Dx: hypoglycemia with acidemia and high lactate
gluconeogenic defect, alcohol induced
76
Diff Dx: hypoglycemia with acidemia and low lactate
glycogenolysis or counterregulation defect
77
Diff Dx: hypoglycemia with high fatty acids
FAO defect
78
Diff Dx: hypoglycemia with low FFA, low ketones, no acidemia
hyperinsulinemic hypoglycemia
79
Key feature of insulin-mediate hypoglycemia
suppressed ketones

Endocrine (26 decks)

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