399 Hypoglycemia Flashcards

1
Q

What is Whipple’s triad

A
  1. symptoms consistent with hypoglycemia 2. a low plasma glucose concentration measures with a precise method 3. relief of symptoms after the plasma glucose is raised
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2
Q

lower limit of fasting plasma glucose concentration

A

About 70 mg/dl or 3.9 mmol

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3
Q

normal plasma glucose range in fasting state

A

70-110 mg/dl or 3.9-61. mmol/L

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4
Q

how long can hepatic glycogen stores sufficient to maintain plasma glucose levels

A

for about 8 hours

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5
Q

Causes of hypoglycemia in ill or medicated patients

A
  1. drugs such as alcohol, insulin or insulin secretatgogue 2. critical illness as in hepatic, renal, cardiac failure, sepsis 3. hormone deficiency as in cortisol, glucagon, and epinephrine 4. non islet cell tumor
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6
Q

causes of hypoglycemia in seemingly well individual

A
  1. endogenous hyperinsulinism, insulinism, functional beta cell disorders, 2. disorders of gluconeogenesis and fatty acid oxidation, 3. exercise, 4. accidental surreptitious or malicious hypoglycemia
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7
Q

conditions when blood glucose is normall less than 70 mg/dl

A

later after a meal, pregnancy, during prolong fasting of more than 24 hrs

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8
Q

In a glucagon deficient individual, what is the most critical physiologic response to hypoglycemia

A

increase in epinephrine

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9
Q

primary glucose counter regulatory hormones

A

alpha cell glucagon and adrenomedullary epinephrine

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10
Q

what does glucagon do during hypoglycemia

A

stimulates hepatic glycogenolysis and gluconeogenesis

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11
Q

what does epinephrine do during hypoglycemia

A

epinephrine also stimulates glycogenolysis and gluconeogenesis but limits peripheral uptake of glucose and stimulates lipolysis

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12
Q

when hypoglycemia is prolonged for 4 hours, what hormons support glucose production and restrict glucose utilization

A

cortisol and growth hormone

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13
Q

True or false. Cortisol and growth hormone play no rule in defense againts acute hyypoglycemia

A

True.

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14
Q

Response to decreasing plasma glucose concentrations. Glycemic threshold. Decrease in cognition

A

less than 2.8 mmol or less than 50 mg/dl

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15
Q

Response to decreasing plasma glucose concentrations. Glycemic threshold. Decrease insulin

A

4.4- 4.7 mmol or 80-85 mg/dl

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16
Q

first defense against hypoglycemia

A

decrease in insulin production

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17
Q

second defense against hypoglycemia

A

increase in glucagon

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18
Q

Response to decreasing plasma glucose concentrations. Glycemic threshold 3.6-3.9 or 65-70 mg/dl.

A

increase in glucagon, increase in epinephrine, increase in cortisol and growth hormone

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19
Q

third defense against hypoglycemia

A

epinephrine

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20
Q

True or false. Neuroglycopenic manifestations of hypoglycemia are the direct results of central nervous system glucose deprivation.

A

True.

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21
Q

The limiting factor in glycemic management of diabetes mellitus

A

hypoglycemia

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22
Q

True or false. Incidence of hypoglycemia is lower in T2DM than in T1DM

A

True.

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23
Q

sole determinant of risk for hypoglycemia

A

relative or absolute insulin excess

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24
Q

loss of the warning adrenergic and cholinergic symptoms that previously allowed the patient to recognize developing hypoglycemia and therefore to abort the episode by ingesting carbohydrates

A

hypoglycemia unawareness

25
Q

Manifested as isolated episodes of hypoglycemia with no decrease in insulin and no increase in glucagon leading to attenuated sympathoadrenal responses to hypoglycemia

A

hypoglycemia associated autonomic failure (HAAF)

26
Q

3 manifestation of HAAF

A

defective glucose counterregulation, recurrent hypoglycemia, hypoglycemia unawareness

27
Q

additional risk factor for HAAF in diabetes

A

impaired renal function resulting in reduced clearance of endogenous and exogenous insulin, classical diabetic autonomic neuropathy and lower HbA1c or lower glycemic goals even at elevated HbA1c levels

28
Q

study that attempts to control in hospital plasma glucose values towards physiologic levels resulted in increased mortality risk

A

SUGAR

29
Q

study where severe hypoglycemia with accompanying serious cardiovascular morbidity and mortality also occur

A

ACCORD and VADT

30
Q

True or false. Severe hypoglycemia can occurs in T1DM and T2DM with HbA1c values of 8-10%

A

True.

31
Q

the mechanism alcohol intake leads to hypoglycemia

A

ethanol blocks gluconeogenesis but not glycogenolysis

32
Q

occurs after several day enthanol binge which the person eat little food with consequent glycogen depletion

A

alcohol induced hypoglycemia

33
Q

True or false. Blood ethanol levels correlate poorly with plasma glucose concentrations

A

True.

34
Q

How does extensive liver destruction cause fasting hypoglycemia

A

liver is the major site of endogenous glucose production

35
Q

how does sepsis lead to hypoglycemia

A

increased glucose utilization is induced by cytokine production in macrophage rich tissue such as the liver, spleen, and lung

36
Q

True or false. Cytokine induced inhibition of gluconeogenesis in the setting of nutritional glycogen depletion, in combination with hepatic and renal hypoperfusion can lead to hypoglycemia

A

True

37
Q

True or false. Hypoglycemia is not a feature of epinephrine deficient state that results from bilateral adrenalectomy when glucocorticoid replacement is adequate nor does it occur during pharmacologic adrenergic blockade

A

True.

38
Q

Why does epinephrine deficient state does not lead to hypoglycemia

A

as long as other counterregulatory systems are intact

39
Q

what is the cause of exercise induced hypoglycemia

A

increased activity of monocarboxylate transporter 1 in Beta cells

40
Q

Differential diagnosis for CBG less than 55 mg/dl. Plasma insulin high, Plasma proinsulin low. Plasma C peptide low. Plasma beta hydoxylate low. No circulating oral hypoglycemic. No antibody to insulin.

A

Exogenous insulin

41
Q

Differential diagnosis for CBG less than 55 mg/dl. Plasma insulin high, Plasma proinsulin high Plasma C peptide high Plasma beta hydoxylate low. No circulating oral hypoglycemic. No antibody to insulin.

A

Insulinoma

42
Q

differential diagnosis for CBG less than 55 mg/dl. Plasma insulin high, Plasma proinsulin high Plasma C peptide high Plasma beta hydoxylate low. With circulating oral hypoglycemic. No antibody to insulin.

A

SU or insulin secretagogue

43
Q

Differential diagnosis for CBG less than 55 mg/dl. Plasma insulin high, Plasma proinsulin high Plasma C peptide high Plasma beta hydoxylate low. No circulating oral hypoglycemic. With antibody to insulin.

A

Insulin autoimmune hypoglycemia

44
Q

when is plasma insulin high

A

more than 3 uU/ml or more than 18 mmol

45
Q

when is plasma C peptide high

A

more than 0.6 ng/ml or more than 0.2 mmol

46
Q

when is plasma proinsulin high

A

more than 5.0 pmol/L

47
Q

when is beta hydoxybutarate low

A

less than 2.7 mmol

48
Q

refers to pattern of diffuse islet involvment with beta cell hypertrophy

A

mesidioblastosis

49
Q

refers to pattern of diffuse islet involvment with beta cell hypertrophy but patients postprandial hypoglycemia

A

noninsulinoma pancreatogenous hypoglycemia

50
Q

used to treat hypoglycemia caused by insulinoma

A

diazoxide, octreotide

51
Q

initial dose of glucose in a patient who is able and willing

A

15-20 g of glucose

52
Q

additional treatment to be given in addition to glucose injection in patients with T1Dm

A

SC or IM glucagon 0.1 mg

53
Q

Why is glucagon injection less useful in T2Dm

A

also stimulate insulin secretion

54
Q

whys is glucagon not useful in alcohol induced hypoglycemia

A

is stimulates glycogenolysis, glucagon is ineffective in glucagon depleted individuals as in alcohol induced hypoglycemia

55
Q

Treatment for hypoglycemia. Autoimmune hypoglycemia

A

Glucocorticoids; immunosuppresive drugs

56
Q

Treatment for hypoglycemia. Nontumor beta cell disorder

A

Partial pancreatectomy

57
Q

Treatment for hypoglycemia. Non resectable insulinoma

A

octreotide; diazoxide

58
Q

Treatment for hypoglycemia.Insulinoma

A

Surgical resection