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Flashcards in Hypoglycemia Deck (79):
1

T/F Hypoglycemia is a diagnosis

F --> sign

2

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

24-36

3

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

glycogenolysis (and a little bit of gluconeogenesis)

4

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

Growth hormone increases

5

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

increases

6

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

increases

7

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

increases

8

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

decreases

9

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

increases

10

Which 2 hormones upregulate glycogenolysis?

glucagon and epinephrine

11

Which 2 hormones upregulate gluconeogenesis?

glucagon and cortisol

12

Which 2 hormones upregulate lipolysis?

epinephrine and growth hormone

13

Which hormone upregulates ketogenesis?

epinephrine

14

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

increase

15

Ketone bodies (2)

beta hydroxybutyrate and acetoacetate

16

What is therapeutic hypoglycemia?

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

17

What is diagnostic hypoglycemia?

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

18

At what glucose level does cognitive dysfunction begin?

45-50 mg/dL

19

Whipple's Triad

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

20

Neurogenic symptoms of hypoglycemia

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

21

Neuroglycopenic symptoms of hypoglycemia

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

22

What comes first, neurogenic or neuroglycopenic symptoms?

neurogenic

23

HAAF

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

24

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

epinephrine

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