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MLSCI 263 > Diabetes Mellitus & Diabetic Ketoacidosis > Flashcards

Diabetes Mellitus & Diabetic Ketoacidosis Flashcards

1
Q

glucose utilization to generate ATP

A
  • anaerobic glycolysi (Embden-Meyerhof cycle)
    glucose = pyruvate + lactate
  • aerobic glycolysis (Krebs or TCA cycle)
    glucose - CO2 + H2O
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2
Q

gluconeogenesis

A

non-sugar sources => glucose-6-phosphate

pyruvate, lactate, AAs, fatty acids => KETOSIS

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3
Q

hormonal control of glucose

A

insulin reduces blood glucose

  • preproinsulin => proinsulin => insulin + (inactive) C peptide
  • synthesis and cleavage within pancreatic B cells of islets of Langerhans
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4
Q

insulin antagonists …

A

increase blood glucose

- epinephrine, growth hormone, cortisol, thyroxine, intestinal hormones (ghrelin stimulates GH release)

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5
Q

stimulates insulin secretion after a meal

A

gastric inhibitory protein (GIP)

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6
Q

these cells on the islets of Langerhans produce insulin

A

pancreatic beta cells

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7
Q

destruction of beta cells result in:

A
  • decrease/no insulin production
  • no secretion into blood
  • type I diabetes
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8
Q

a metabolic disorder characterized by presence of hyperglycemia due to defective insulin secretion, insulin or both

A 
diabetes mellitus (DM0; 4 types based on cause)
type I, II, gestational, specific ...
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9
Q

type I diabetes

A
  • B cell destruction (insulin def)
  • prone to ketosis
  • autoimmune: Abs present in most or idiopathic
  • onset at any age: 75% before 18 y/o
  • ABRUPT onset of symptoms:
    > polyuria
    > polydipsia
    > rapid weight loss (high [glucose] but can’t enter cells; gluconeogenesis so ketosis)
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10
Q

type II diabetes

A
  • impaid insulin action
  • [insulin] may be N, decreased, increased; not prone to ketosis
  • predominant insulin resistance; relative insulin def
  • OR predominant secretory defect with insulin resistance
  • onset at any age; commonly after 40 y/o; emerging in teens and children
  • onset of symptoms: obesity (poor diet, inactive lifestyle)
  • 90%; more common; not insulin-dependent mostly
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11
Q

T or F. type I diabetes is 5-10% of incidences and all are insulin-dependent

A

T

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12
Q

gestational diabetes

A
  • glucose intolerance with onset or first recognition of pregnancy (excludes diabetic women who become pregnant)
  • unable to produce insulin required = hyperglycemia (placental hormones block action of insulin in mother)
  • usually c lears after delivery
  • increases risk of type teoo diabetes of mom later in life (esp. with marked hyperglycemia, obesity, or diagnosis prior to 24 wks)
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13
Q

specific types of diabetes due to other causes …

A
  • underlying genetic defects: beta cell function, pancreatic diseases (CF)
  • endocrine diseases (Cushing’s syndrome, acromegaly)
  • other genetic conditions: Down’s syndrome, Klinefelter’s syndrome
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14
Q

consequences of gestational diabetes to baby

A

mother’s insulin does not cross body but glucose does so baby pancreas just make more insulin = extra E stored as fat = macrosomia (larger baby)

  • complications in delivery
  • higher risk of breathing probs
  • neonatal hypoglycemia
  • increased risk of obesity in childhood and type II DM in adulthood
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15
Q

why use HbA1c to diagnose diabetes mellitus?

A
  • patient preparation (not fasting)
  • HbA1c methods standardized
  • HbA1c better for long-term hyperglycemia
  • correlates better with compilation
  • minimal influence from Hb variants
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16
Q

glycated form of HbA0

A

HbA1

17
Q

quantitaation of HbA1c

A
  • ion exchange HPLC: detects different Hbs, HbF slower glycation rate; measure total glycated Hb/non-glycated Hb
  • HPLC STD: calibration std, chromatographic peak (IFCC: glucose adduct to the valine of the beta chain of Hb)
17
Q

quantitaation of HbA1c

A
  • ion exchange HPLC: detects different Hbs, HbF slower glycation rate; measure total glycated Hb/non-glycated Hb
  • HPLC STD: calibration std, chromatographic peak (IFCC: glucose adduct to the valine of the beta chain of Hb)

HbA1c-specific immunoassays: MOST COMMON, Abs to 4-1o AA on N-terminal valine; some methods affected by mutation in HbS or HbC wwhoch may be close to N-terminus

18
Q

this monitors glycemic control

A

glycated hemoglobin

  • every three months (treatment goal <7.0%)
  • reflects blood glucose over previous 90 days; rBC lifespan 120 days
  • mean values predict progression of complications = retinopathy, nephropathy, neuropathy
  • major test used to monitor glycemic control
19
Q

why is glycated Hb the major test used to monitor glycemic control?

A
  • reinforce self-glucose monitoring
  • reassure patient program is working
  • evaluate newly diagnosed diabetocs
  • question patient or glucometer reliability
20
Q

T or F. hyperglycemia happens with just diabetes

A

F!

  • Cushings syndrome
  • Phepochromocytomas of the adrenal medulla
  • primaaary aldosteronism
  • hyper or hypothyroidism
  • acromegaly (GH antagonist)
  • acute pancreatitis
  • cerebral lesipoons
  • CO poisoning
  • lipoproteinemia
  • liver disease
21
Q

hypoglycemia

A
  • pancreative islet cell tumor (too much insulin produced)
  • insulin overdose
  • inefficiency in antagonist to insulin hormones
  • prolonged carb deprivation
  • certain non-insulin producing tumors
22
Q

diagnosing hypoglycemia

A
  • fasting hypoglycemia: stress testing: prolonged fast (72 h, done in hospital); random glucose measurement
- postprandial hypoglycemia: measures blood glucose wen symptoms occur and relief of symptoms when glucose values return to normal 
 > alimentary - dumping syndrome
 > sub-clinical diabetes mellitus
 > alcoholism
 > functional hypoglycemia
23
Q

idiopathic hypoglycemia of infancy

A

occurs within 72h of birth: tremors, twitching

24
Q

leucine sensitivity

A
  • usualy within first 2 y of life and resolved by 5 y/o

- leucine-roch food => overproduction of insulin

25
Q

nesidioblastosis

A

pancreatic islet cell hyperplasia

26
Q

galactosemia

A

inborn error: galactose does NOT get made into glucose

27
Q

ketosis

A
  • onset age 1.5-5y, disappears by age 10
  • prolonged lack of food, or low CHO diet
  • more common in males of lower birth weight and kids in low socioeconomic groups
28
Q

neonatal and early childhood hypoglycemia (5)

A
  • idiopathic hypoglycemia of infancy
  • leucine sensitivity
  • nesidioblastosis
  • galactosemia
  • ketosis
29
Q

diabetic ketoacidosis (DKA)

A
  • acute life-threatening medical emergency due to an absolute or relative deficiency in insulin arising from:
    > failure of endogenous insulin secretion (new onset)
    > inadequate administration of insulin
    > increased requirement for insulin

major threat: osmotic diuresis, dehydration
no glucose enters cells = increase in blood glucose

30
Q

clinical features of ketoacidosis

A
  • polyuria
  • polydipsia
  • weakness
  • nausea, vomitting
  • dry skin
  • fruity sweet odour on breath (acetone)
31
Q

factors contributing to development of ketoacidosis

A
  • 40% infection
  • 25% missed insulin dose
  • 15% previously unknown, new onset DM
  • 20% other causes:
    > insulin resistance
    > emotional/physical trauma
    > insufficient fluid intake in hot weather
    > heart attack or store
    > alcohol or drug abuse
    > pancreatitis
    > thyroid crisis
32
Q

most important test or indication of diabetic ketoacidosis

A

elevated beta hydroxybutyrate = replaced other tests

33
Q

test choice for diagnosis of DKA

A

beta hydroxybutyrate
> specifity and sensitivity supeiror to other methods
> test availability on instments has improved
> point of care instrument available

34
Q

for a comatose patient with possible diabetes. perform serum beta-hydroxybutyrate test =

A
  • positive = diabetic ketoacidosis

- negative = consider other causes

MLSCI 263 (31 decks)

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