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Glycemic states Flashcards

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1
Q

Stimulants of insulin release

A

glucose (major)
amino acids (arginine, leucine)
PSNS, GIP, GLP, glucagon

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2
Q

inhibitors of insulin release

A

SNS

somatostatin

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3
Q

effects of insulin - general

A

facilitates glucose (GLUT4) and amino acid uptake into cells
inhibits gluconeogenesis, glycogenolysis, lipolysis
increases rate of protein synthesis and decreases rate of degradation

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4
Q

Effects of insulin - muscle

A

stimulates glycogenesis

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5
Q

Effects of insulin - adipocyte

A

stimulates conversion of FFAs ans glucose –> TGs

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6
Q

Effects of insulin - liver

A
  • stimulates glycogenesis by activation of glycogen snthase
  • stimulates glycolysis by activation of glucokinase, phosphofructokinase, pyruvate kinase
  • inhibits glycogenolysis by inactivation of glycogen phosphorylase
  • inhibits gluconeogenesis by inhibition of pyruvate carboxylase, phosphenol pyruvate carboxykinase (PEPCK) and fructose 1,6 diphosphatase
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7
Q

Stimulants of glucagon release

A

SNS, PSNS, GIP, CCK, amino acids (arginine and alanine)

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8
Q

Inhibitors of glucagon release

A

insulin, somatostatin, GLP, glucose, Islet amyloid polypeptide (secreted with insulin from B-cells, acts to retard gastric emptying and glucagon secretion, helps to control blood glucose sparing insulin)

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9
Q

Glucagon effects on metabolism

A

Inhibits glycogenesis, TG synthesis, hepatic protein synthesis
Stimulates gluconeogenesis via increased uptake of gluconeogenic amino acids; inhibition of pyruvate kinase, and stimulation of PEPCK and pyruvate carboxylase
Stimulates glycogenolysis via glycogen phosphorylase
Stimulates fat breakdown and hepatic (NOT MUSCLE) protein breakdown
enhances ketogenesis

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10
Q

Epinephrine effects on metabolism

A

Stimulates glycogenolysis, gluconeogenesis, glucagon release, lipolysis
Inhibits insulin release

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11
Q

Effects of cortisol on metabolism

A

stimulates gluconeogenesis, lipolysis, protein degradation

inhibits glucose uptake by muscle and adipose tissue

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12
Q

Effects of GH on metabolism

A

stimulates lipolysis and promotes protein synthesis

inhibits glucose uptake by muscle and decreases rate of protein degradation

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13
Q

GH stimulant

A

Ghrelin

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14
Q

Causes of hyperglycemia

A 
Endocrine:
- diabetes
- acromegaly
- Cushing's
- glucagonoma
- somatostatinoma
- pheochromocytoma
Pancreatic insufficiency - chronic pancreatitis, hemochromatosis, subtotal pancreatectomy
Drugs: GCs, thiazides, phenytoin, niacin, OCP
Others: gestational diabetes, cirrhosis
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15
Q

Hypoglycemia causes

A

Reactive/postprandial/functional hypoglycemia
- can be normal or due to post gastrectomy, galactosemia, hereditary fructose intolerance
Excess use of insulin/sulfonylurea
Acute alcohol intoxication - suppress gluconeogenesis
Drugs: salicylates, quinine, propoxyphene, disopyramide, propanolol, MAOIs
Hyperinsulinism: insulinoma, hyperplasia of beta cells, inherited defects of Katp channels
Endocrine: adrenal failure, panhypopituitarism, isolated ACTH/GH deficiency
Liver failure
Renal failure
Non-pancreatic neoplasms: increased IGF2
Neonatal disorders (glycogen storage, etc)
Septicema

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16
Q

Insulin synthesis and processing

A

1) Proinsulin synthesized in beta cells
- A and B chains linked by -S-S-
- C-peptide
2) Proinsulin processed efficiently in granules by prohormone convertase enzymes (PC1/3 and PC2), and carboxypeptidase E –> Insulin and C-peptide
3) Insulin crystallizes with Zinc in granule centre; C peptide in granule halo

  • C-peptide no known function, but a good marker for endogenous insulin secretion
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17
Q

Insulin receptor

A

Tyrosine kinase enzyme (glycoprotein)
on muscle, adipose, and liver tissue
2 alpha - extracellular, linked by -S-S-
2 beta - transmembrane, dip into cytoplasm, each linked to alpha by -S-S-

1) Binds insulin –> conformational change
2) stimulates TK activity in beta units
3) autophosphorylation of receptor
4) phosphorylation of other intracellular proteins
5) various actions - e.g. translocation of GLUT4 onto surface

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18
Q

Consequences of insulin deficiency

A

Hyperglycemia
Increased FA in blood
Protein catabolism

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19
Q

Consequences of insulin excess

A

Reverse metabolic changes
First symptoms:
- palpitations, sweating, nervousness
Lower plasma glucose levels: confusion, other cognitive abilities
Even lower: lethargy, coma, convulsions, eventually death

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20
Q

Newborn hypoglycemia

A

Common in critically ill or extremely low birthweight infants
Most cases - multifactorial, transient and easily supported.
Some cases: due to hyperinsulinism, hypopituitarism, or an inborn error of metabolism

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21
Q

Causes of transient newborn hypoglycemia

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A

Prematurity, intrauterine growth retardation, perinatal asphyxia
Maternal hyperglycemia due to diabetes or iatrogenic glucose administration
Sepsis
prolonged fasting

22
Q

Hypoglycemia in young children

Study These Flashcards
A

Gastroenteritis/fasting

Recurrent - inborn error of metabolism, congenital hypopituitarism, or congenital hyperinsulinism

23
Q

Hypoglycemia in young adults

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A

Most common: injected insulin for type 1 diabetes
Congenital causes would have manifested before this age
Body mass large enough - starvation/idiopathic ketotic hypoglycemia less common
Addison’s disease
Sepsis

24
Q

Hypoglycemia in older adults

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A 
Complex drug interactions
Insulinoma, other tumours
Acquired adrenal insufficiency
Acquired hypopituitarism
Immunopathologic hypoglycemia
25
Carinitine level during hypoglycemia
Should be increased due to increased lipolysis and ferrying of FFAs to the mitochondria may be low in FA oxidation disorders
26
Amino acid levels during hypoglycemia
should be decreased due to increased gluconeogenesis (esp essential amino acids) Abnormal: suggests certain inborn errors of amino acid metabolism or gluconeogenesis
27
Somatostatin indication
suppression of hormones or transmitters in: - islet cell tumours (insulinoma, glucagonoma) - acromegaly - symptomatic VIP/carcinoid tumours
28
Somatostatin MOA
secreted by delta cells of the pancreatic islet inhibits release of: insulin (via inhibition of CaV), glucagon, GH, gastrin, VIP causes v/c leading to reduced portal venous flow
29
Glucagon indication
refractory hypoglycemia (not corrected by glucose)
30
Glucagon MOA
endogenous peptide hormone , counter regulatory Main effects on the liver: increase glycogenolysis, decrease glycogenesis, increase glycolysis, increase ketogenesis Positive ionotropic and chronotropic effect on cardiac tissue Stimulates endogenous insulin secretion Inhibited by insulin and somatostatin
31
Diazoxide MOA
prolongs opening of ATP sensing K+ channel in beta cells, inhibits pancreatic secretion of insulin
32
Diazoxide indications
parenteral use as an antihypertensive | orally antihypoglycemic agent secondary to hyperinsulinemia
33
Glucokinase mutation
dominant inheritance regulatory mutation leads to hyperinsulinism
34
Glutamate dehydrogenase mutation
dominant | leads to hypoglycemia and hyperinsulinism and hyperammonemia
35
G6phosphatase deficiency
Glycogen storage disease, gluconeogenesis disorder critical enzyme in the generation of all new glucose from within the straight chains of glycogen Can get hepatomegaly, high levels of serum triglycerides elevated plasma lactate can also lead to metabolic acidosis Can get hypophosphatemia Minimal ketosis compared to lactic acid buildup
36
Amino 1,6 glucosidase deficiency
Glycogen storage disease hepatomegaly hypoglycemia have capacity to undergo gluconeogenesis
37
Liver phosphorylase and phosphorylase kinase deficiency
Glycogen storage disease Phosphorylase complex ultimately results in teh degradation of the straight chains of liver glycogen
38
Glycogen synthase deficiency
Glycogen storage disease
39
Fructose 1,6 diphosphatase deficiency
gluconeogenesis disorder results in a block of gluconeogenesis from all possible precursors below the level of fructose 1,6 diphosphate results in lactic acidosis glycogenolysis remains intact
40
PEP carboxykinase deficiency
gluconeogenesis disorder
41
Galactosemia
Galactose --> phosphorylated --> conjugated + uridine --> UDP galactose --> epimerization to UDP glucose Galactose restricted diet Deficiencies: galactose-1-phosphate uridyl rtansferase UDP-galactose-4-epimerase
42
Fructose-1-phosphate aldolase
results in hereditary fructose intolerance
43
Newborn short hypoglycemia management
take critical blood sample | then glucagon 1 mg im/iv
44
Cause of neonatal fasting hypoglycemia with lactic acidosis
Can be normal G6Pase, FDPase, Pyruvate carboxylase deficiency Test for gluconeogenic precursors Glucagon stimulation test
45
Causes of neonatal fasting hypoglycemia with ketoacidosis
Normal GH deficiency Cortisol deficiency Test for adrenal and pituitary function glucagon stimulationt est
46
Causes of fasting hypoglycemia with no ketosis
Elevated FFA: FA oxidation disorders, normal do acyl-carinitine profile Low FFA: hyperinsulinism, panhypopituitarism, SGA, birth asphyxia - glucagon stimulation test - pituitary, adrenal and thyroid function - insulin assay - other tests for HI
47
Infant glucose requirement
6-8 mg/kg /min - larger requirement, high brain-to-body ratio Prone to hypoglycemia due to small stores mobilization of glycogen stores initiated at cutting of umbilical cord
48
Adult glucose requirement
3.4 mg /kg /min
49
Insulin secretion mechanism
1) glucose uptake via GLUT 2 2) metabolized, ATP produced 3) increased ATP/ADP --> K-ATP channel closes, depolarization 4) CaV opens, Ca influx --> insulin granule exocytosis 5) Ca also activates gene expression via CREB
50
Acute symptomatic neonatal/infant hypoglycemia treatment
iv D10W infusion, then continuous glucose infusion | If hypoglycemic seizures present --> more D10W bolus
51
Management of persistent neonatal/infantile hypoglycemia
Increase rate of iv glucose to 10-15 mg/kg/min or more if needed Hyperinsulinemia --> diazoxide, then octreotide Hypoglycemia unresonposive to glucose + diazoxide/octreotide --> consider partial/near-total pancreatectomy Continued prolonged medical therapy without pancreactic resection if hypoglycemia is favourable, due to spontaneous recovery in some cases Total pancreatectomy not optimal: risk of surgery, permanent DM, exocrine pancreatic insufficiency

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