Hypoglycemia Flashcards

1
Q

Hypoglycemia Sxs

A
  • At 80mg/dl insulin release declines, at 65-70 glucagon and epinephrine release is triggered, and <50): confusion, lethargy, stupor, combativeness
  • And lower than 30: loss of conscience, seizure, death
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2
Q

Whipples triad

A
  • A description of hypoglycemia: low blood sugar, w/ Sx of hypoglycemia that is reversed w/ returning the glc to normal levels
  • Most of the Sx are first caused by autonomic (sympathoadrenal) activation, then by neuroglycopenia
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3
Q

Pathogenesis of hypoglycemia

A
  • Hypoglycemia happens when there is: inadequate substrate for GNG and FA production
  • Liver function is not adequate to perform GNG and FA oxidation
  • Hormone deficiencies preventing the induction of key GNG nzs
  • Inappropriate levels of insulin/IGF which prevents hepatic glc production and/or stimulate excessive glc utilization by muscle
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4
Q

Pts at risk for hypoglycemia

A
  • Mostly pts being treated for diabetes (both T1 and T2), also those who are pre diabetic and have insulin resistance
  • T2 diabetics can still make glucagon (T1 can’t) and thus are much less likely to get hypoglycemic than T1
  • Usually due to high insulin levels (most often exogenous)
  • Rare causes: insulinomas
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5
Q

Causes of hypoglycemia

A
  • Healthy appearing: drugs (etoh, salicylates, quinine, haloperidol), insulinoma, islet cell hyperplasia/nesidioblastosis (islet cell hyperplasia in infants), insulin abuse, intense activity
  • Ill appearing: shock, insulin (IV, SQ), pentamindine, bactrim, childhood diseases, hypopituitarism, hypoadrenalism, ACTH deficiency, tumors, starvation/anorexia
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6
Q

Counter-regulatory mechanisms for hypoglycemia

A
  • In order of first to last after hypoglycemia begins
  • Glucagon release (60 mg/dl glc): stimulates glycogenolysis, lipolysis, GNG, suppresses insulin release
  • Adrenaline (60): decreases peripheral utilization of glc and stimulates GNG and lipolysis in liver
  • Cortisol/GH (40): decreases peripheral utilization of glc and enhances glc production by the liver
  • These responses are triggered by: receptors in CNS to glc levels, hypoglycemia itself stimulates glucagon, glc sensors in liver
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7
Q

Impaired counter-regulatory responses in diabetes 1

A
  • T1: T1 diabetics have reduced glucagon response soon after developing DM (probably from heavily relying on exogenous insulin), thus the pts rely on autonomic responses to maintain high enough glc levels
  • Eventually the autonomic response is also blunted and they develop hypoglycemia unawareness where they no longer experience the warning Sx of early hypoglycemia
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8
Q

Impaired counter-regulatory responses in diabetes 2

A
  • T2: more likely to complain of feeling unwell at normal glc levels (altered glycemic threshold)
  • This is b/c if blood glc levels have been running high for a long time a new homeostasis is established and the pt acclimates to the high glc level
  • These pts will report feeling unwell when glc is around the low 100s, and they will have an exaggerated adrenaline response when glc gets to 80-90
  • This is thought to be due to down-regulation of glc receptors in the brain and can be reversed if they control their glc and do not treat the Sx unless the glc falls below 80
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9
Q

Rx of hypoglycemia

A
  • 10-15g of glucose should be given, the best is 4oz of a regular caffeinated soda (1/2 a normal can)
  • After 10 min the glc levels should be checked, if there is no improvement then repeat glc administration
  • If there are 3 glc administrations and no improvement they need to be hospitalized (for IV glc)
  • Avoid using complex cards since they are less easily digested and utilized, sugary drinks are best
  • Glucagon injections can work if the person does it correctly
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