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4 > Glycemic states > Flashcards

Glycemic states Flashcards

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

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

A

Gastroenteritis/fasting

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

23
Q

Hypoglycemia in young adults

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

A 
Complex drug interactions
Insulinoma, other tumours
Acquired adrenal insufficiency
Acquired hypopituitarism
Immunopathologic hypoglycemia
25
Q

Carinitine level during hypoglycemia

A

Should be increased due to increased lipolysis and ferrying of FFAs to the mitochondria
may be low in FA oxidation disorders

26
Q

Amino acid levels during hypoglycemia

A

should be decreased due to increased gluconeogenesis (esp essential amino acids)
Abnormal: suggests certain inborn errors of amino acid metabolism or gluconeogenesis

27
Q

Somatostatin indication

A

suppression of hormones or transmitters in:

  • islet cell tumours (insulinoma, glucagonoma)
  • acromegaly
  • symptomatic VIP/carcinoid tumours
28
Q

Somatostatin MOA

A

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
Q

Glucagon indication

A

refractory hypoglycemia (not corrected by glucose)

30
Q

Glucagon MOA

A

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
Q

Diazoxide MOA

A

prolongs opening of ATP sensing K+ channel in beta cells, inhibits pancreatic secretion of insulin

32
Q

Diazoxide indications

A

parenteral use as an antihypertensive

orally antihypoglycemic agent secondary to hyperinsulinemia

33
Q

Glucokinase mutation

A

dominant inheritance
regulatory mutation
leads to hyperinsulinism

34
Q

Glutamate dehydrogenase mutation

A

dominant

leads to hypoglycemia and hyperinsulinism and hyperammonemia

35
Q

G6phosphatase deficiency

A

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
Q

Amino 1,6 glucosidase deficiency

A

Glycogen storage disease
hepatomegaly
hypoglycemia
have capacity to undergo gluconeogenesis

37
Q

Liver phosphorylase and phosphorylase kinase deficiency

A

Glycogen storage disease
Phosphorylase complex
ultimately results in teh degradation of the straight chains of liver glycogen

38
Q

Glycogen synthase deficiency

A

Glycogen storage disease

39
Q

Fructose 1,6 diphosphatase deficiency

A

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
Q

PEP carboxykinase deficiency

A

gluconeogenesis disorder

41
Q

Galactosemia

A

Galactose –> phosphorylated –> conjugated + uridine –> UDP galactose –> epimerization to UDP glucose
Galactose restricted diet

Deficiencies: galactose-1-phosphate uridyl rtansferase
UDP-galactose-4-epimerase

42
Q

Fructose-1-phosphate aldolase

A

results in hereditary fructose intolerance

43
Q

Newborn short hypoglycemia management

A

take critical blood sample

then glucagon 1 mg im/iv

44
Q

Cause of neonatal fasting hypoglycemia with lactic acidosis

A

Can be normal
G6Pase, FDPase, Pyruvate carboxylase deficiency

Test for gluconeogenic precursors
Glucagon stimulation test

45
Q

Causes of neonatal fasting hypoglycemia with ketoacidosis

A

Normal
GH deficiency
Cortisol deficiency

Test for adrenal and pituitary function
glucagon stimulationt est

46
Q

Causes of fasting hypoglycemia with no ketosis

A

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
Q

Infant glucose requirement

A

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
Q

Adult glucose requirement

A

3.4 mg /kg /min

49
Q

Insulin secretion mechanism

A

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
Q

Acute symptomatic neonatal/infant hypoglycemia treatment

A

iv D10W infusion, then continuous glucose infusion

If hypoglycemic seizures present –> more D10W bolus

51
Q

Management of persistent neonatal/infantile hypoglycemia

A

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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