B2. 046 Prework 2 Overview of Diabetic Ketoacidosis Flashcards

1
Q

ketosis

A

a normal metabolic process in which body produces ketone bodies in the liver for the utilization by peripheral tissues

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2
Q

ketonemia

A

abnormally high concentration of ketone bodies in the blood

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3
Q

ketonuria

A

abnormally large amount of ketone bodies in the urine

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4
Q

ketoacidosis

A

a serious complication of diabetes caused by over production of ketone bodies by the liver coupled with under utilization of ketone bodies by peripheral tissues

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5
Q

fatty acid oxidation

A

conversion of fatty acids to acetyl CoA by beta oxidation

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6
Q

ketogenesis

A

liver pathways that converts two molecules of acetyl CoA into B-hydroxybutyrate at the expense of one molecule of NADH

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7
Q

ketolysis

A

pathways in tissues other than the liver in which ketone bodies are oxidized to acetyl CoA and then to CO2 and H2O by the citric acid cycle

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8
Q

citric acid cycle

A

cyclic conversion of acetyl CoA into 2 molecules of CO2 with the production of 3 NADH, 1 FADH2, and 1 GTP

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9
Q

what are the ketone bodies?

A

acetoacetic acid
B-hydroxybutyric acid
acetone

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10
Q

why can acetone be detected on the breath of some individuals?

A

high concentrations of acetoacetate in the blood break down into acetone and CO2 which are exhaled

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11
Q

how is metabolic ketoacidosis prevented in normally functioning individuals?

A

ketone bodies produced from fatty acids by the liver are oxidized to CO2 and H2O in peripheral tissues

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12
Q

why can excretion of acetoacetate and B-hydroxybutyrate in the urine be detrimental?

A

excretion of these ketone bodies is accompanied by Na+ ions to maintain electrical neutrality
this exacerbates metabolic acidosis because it leaves H+ in the blood that cannot be removed by simply oxidizing the ketone bodies

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13
Q

what are the two primary causes of metabolic acidosis?

A

ketoacidosis

lactic acidosis

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14
Q

what is the anion gap?

A

detects high concentrations of organic acids in the blood

Na-(Cl+HCO3)

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15
Q

what is the rate limiting enzyme for fatty acid oxidation?

A

CPT1

totally active when insulin is absent

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16
Q

what is the negative allosteric effector of CPT1?

A

malonyl CoA

17
Q

why is malonyl CoA reduced in a starved/DM1 state?

A

acetyl CoA carboxylase is inhibited by long chain acyl esters produced from FFAs and phosphorylated/deactivated by glucagon