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Biochem final > Quan > Flashcards

Quan Flashcards

1
Q

essential for life in all aerobic organisms

A

oxygen

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2
Q
  • retards aging in human cells
  • relieves headaches
  • boosts immune system
  • improves physical performance
A

oxygen

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3
Q

inert at body temperature

A

oxygen

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4
Q

oxygen reactivity requires:

A

high heat (activation energy)

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5
Q

oxygen is activated at body temperature by:

A

metal ions (iron, copper, manganese)

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6
Q

loss of elections and increase in oxidation state

A

oxidation

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7
Q

gain of electrons and decrease in oxidation state

A

reduction

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8
Q

partially reduced, reactive form of oxygen

A

reactive oxygen species (ROS)

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9
Q

most prevalent ROS in the blood and tissues, stable molecule unless reacted with metal

A

H202 (hydrogen peroxide)

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10
Q

most reactive and damaging species

A

OH radical

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11
Q

cluster of atoms, one which contains an unpaired electron in its outermost shell of electrons

A

free radical

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12
Q

1) Reaction of oxygen with decompartimentalized metal ions (fenton and harber weiss rxns)
2) As a side reaction of mitochondrial electron transport
3) Normal enzymatic reactions (formation of H2O2 by fatty acid oxidases in the peroxisome)

A

3 mechanisms ROS formed by

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13
Q

occurs when the rate of ROS generation exceeds the ability to neutralize them

A

oxidative stress

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14
Q

results in an increase in oxidative damage to biomolecules

A

oxidative stress

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15
Q

used by immune cells to destroy pathogen, also a feature of inflammatory disease

A

ROS

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16
Q

how does ROS damage cells

A

thru pathway of lipid peroxidation, resulting in advanced lipoxidation end products

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17
Q

one of most sensitive sites of ROS damage, PUFA’s readily react with ROS

A

cell membrane

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18
Q

leads to reduced integrity and function; ion gradients disrupted and asymmetry of phospholipid bilayer (apoptosis)

A

ROS damage to cell membrane

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19
Q

2 amino acids very susceptible to oxidation by the action of ROS

A

cysteine and methionine

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20
Q

most common DNA lesion

A

8-OH-G

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21
Q

reacts with all components of the DNA molecule, damaging both purine and pyrimidine bases along with deoxyribose backbone

A

hydroxyl radical

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22
Q

represents the first step involved in mutagenesis, carcinogenesis, and aging

A

permanent modification of genetic material from oxidative damage

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23
Q

limiting function is important for reducing oxidative damage, but it is also essential for fxn of cells

A

ROS

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24
Q

the cells of what gland must make hydrogen peroxide to attach iodine atoms to thyroglobulin in the synthesis of thyroxine?

A

thyroid gland

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25
Q

must generate ROS in order to kill some types of bacteria that they engulf by phagocytosis

A

macrophages and neutrophils

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26
Q

superoxide dimutase and catalase (CAT)

A

enzymatic defenses against ROS

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27
Q

converts 2 superoxide anions into a molecule of hydrogen peroxide and one of oxygen

A

superoxide dimutase (SOD)

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28
Q

converts hydrogen peroxide to water and oxygen

A

catalase (CAT)

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29
Q

both dimutases, catalyzing oxidation and reduction of separate substrate molecules; both highly specific for their substrates O2 and H2O2

A

superoxide dimutase and catalase (CAT)

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30
Q

small molecules that are antioxidants; vitamin A, C, E, uric acid

A

antioxidant defenses against ROS

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31
Q

major energy sources in the body?

A

glucose and fatty acids

32
Q

fuels brain activity, continuous supply is essential for survival

A

glucose

33
Q

preferred source in muscle, used during initial exercise

A

glucose

34
Q

stored as glycogen in liver and muscle to be released quickly

A

glucose

35
Q

long term energy store?

A

fatty acids

36
Q

supports energy needs during prolonged fasting, unlimited capacity, higher energy source that carbs or protein

A

fatty acids

37
Q

can you use amino acids as energy source?

A

yes, during fasting or metabolic stress

-excess ingestion in diet, converted to carbs and stored

38
Q

pasma glucose concentration is the result of?

A

intake, production, tissue utilization

39
Q

secreted by beta cells

A

insulin

40
Q

secreted by alpha cells

A

glucagon

41
Q

insulin dependent glucose entry into cells is mediated by:

A

glucose transporters (GLUT4)

42
Q
  • controls glucose uptake in skeletal muscle and adipocytes

- most molecules reside intracellularly and no more than 10% in PM

A

GLUT4

43
Q

in humans, doubles the recruitment of the transporter GLUT4 into the cell membrane

A

insulin

44
Q

muscular contraction _____ the expression of GLUT4 independently of insulin

A

increases

45
Q

fatty acids ____ the expression of GLUT4 in muscle

A

decrease

46
Q

promotes anabolism in the liver, adipose tissue, and muscle

A

insulin

47
Q

cause of type 2 diabetes?

A

insulin resistance

48
Q

due to inadequate synthesis, secretion, most commonly unable to exert normal effect

A

insulin resistance

49
Q

receptor binding compromised, mutation in receptor gene, anti receptor autoantibodies, signaling defects in IRS kinase pathway

A

defect in insulin signaling caused by insulin resistance

50
Q
  • mobilizes glucose
  • increases blood glucose
  • stimulates catabolism
  • suppresses anabolism
A

glucagon

51
Q

a catecholamine, acts in signaling through receptors

A

epinephrine

52
Q
  • inhibits glycolysis and lipogenesis

- stimulates gluconeogenesis

A

epinephrine

53
Q

phosphorylation usually stimulates enzymes in _____ and inhibits those in anabolic ones

A

catabolic pathways

54
Q

causes of hypoglycemia:

A

exercise, fasting, excess of exogenous insulin, isulinoma (xs of endogenous insulin), inhibition of endogenous glucose production

55
Q

high insulin/low glucose; while eating and for several house after

A

fed state

56
Q

low insulin/high glucagon; while fasting between 6-12 hrs

A

fasting state

57
Q

chronic low insulin/ high glucagon during fasting over 12 hours

A

starvation state

58
Q

substrates for gluconeogenesis

A

lactate, alanine, glycerol

59
Q

major energy substrate during prolonged starvation (after 12 hours)

A

free fatty acids

60
Q

allows for the recycling of lactate back to glucose, but does not contribute to de novo synthesis of glucose

A

cori cycle

61
Q

increases as fasting continues

A

glucose contribution from gluconeogenesis

62
Q

____ of glucose comes from glycogen, remainder from gluconeogenesis

A

65-75%

63
Q

anti-insulin hormones

A

epinephrine, glucagon, cortisol

64
Q

drive response to physiological and physical stress (trauma, burns, surgery, infection)

A

anti-insulin hormones

65
Q

stress response to PRESERVE glucose supply, induces insulin resistance

A

anti insulin hormones

66
Q

decreased metabolism response to stress:

A

decreases ANABOLISM (glycogen synthesis, lipogenesis, glucose uptake for more brain utilization)

67
Q

increased metabolism response to stress:

A

increased CATABOLISM (glycogenolysis, gluconeogenesis, lipolysis, proteolysis, insulin dependent glucose uptake)

68
Q
  • develops before age 45
  • characterized by destruction of beta cells
  • inherited disease
A

type 1 diabetes

69
Q

prone to ketoacidosis and dependent on insulin

A

type 1 diabetes

70
Q
  • often develops in obese people over 40
  • involves insulin resistance and impaired insulin secretion
  • strong hereditary link
  • ketoacidosis is rare
A

type 2 diabetes

71
Q

macroanhiopathy is more prevalent (leading to CVD, stroke)

A

type 2 diabetes

72
Q

ketogenesis is activated, lipolysis increases acetyl coA (to feed into ketogenesis), ketone bodies accumulate in plasma

A

diabetic ketoacidosis

73
Q

due to increase in blood H+ by ketone bodies, therefore lowering blood pH

A

diabetic ketoacidosis

74
Q

role of obesity in diabetes

A
  • obesity linked to insulin resistance
  • when increase insulin fails to overcome insulin resistance, plasma glucose increases
  • process can often be revered with weight loss and exercise
75
Q
  • hemoglobin can be modified by glycation
  • degree of glycation is an indicator of glucose exposure over RBC lifespan
  • normal levels is 4-6%
A

A1C test

76
Q

treatment for diabetes?

A
  • diet and exercise
  • maintenance of blood glucose
  • use of insulin for type 1
  • treatment with oral hypoglycemic drugs (for type 2)

Biochem final (3 decks)

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