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Biochem Exam 3 > Quan Study Guide > Flashcards

Quan Study Guide Flashcards

1
Q

What are the most important functions of oxygen?

A

essential for all aerobic organisms (oxidative phosphorylation

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2
Q

What happens to oxygen at high temps? body temp?

A 
High = highly combustible
Body = inert
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3
Q

What is oxidation?

A

loss of electrons leading to an increase in oxidation state

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4
Q

What is reduction?

A

gain of electrons leading to a decrease in oxidation state

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5
Q

What are ROS?

A

reactive oxygen species which are oxygen molecules (sometimes connected to other atoms) that have one lone e-
(partially reduced reactive forms of oxygen)

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6
Q

What are free radicals?

A

cluster of atoms, one of which contains unpaired electron in outermost shell of electrons
- quickly react with other molecules to obtain a stable configuration

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7
Q

What occurs in the reduction of O2?

A

1st reduction results in superoxide (O2 with free radical)
2nd reduction results in hydrogenate peroxide
Others include hydroxyl radical (OH), hypochlorite ion and hydroperoxyl radical

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8
Q

How are ROS formed?

A
  1. reaction of O2 with decompartmentalized metal ions (Fenton or haber-weiss reaction)
  2. As a side reaction of mitochondrial electron transport
  3. Normal enzymatic reactions
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9
Q

When does oxidative stress occur?

A

when rate of ROS generation exceeds the ability to neutralize them

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10
Q

How do ROS damage cells?

A

lipid peroxidation

  • causes damage to main cellular components
  • cell membrane one of most sensitive sites to ROS damage
  • cysteine and methionine susceptible to oxidation by ROS
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11
Q

What are the physiological functions of ROS?

A
  • Cells of thyroid must make H2O2 to attach iodine atoms to thyroglobulin to make thyroxine
  • macrophages and neutrophils must generate ROS to kill some types of bacteria
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12
Q

What are some defense mechanisms against ROS?

A
  1. preventative mechanisms
  2. repair mechanisms
  3. physical defenses
  4. enzymatic
    - superioxide dismutase converts 2 superoxide anions to hydrogen peroxide and O2
    - catalase converts hydrogen peroxide to water and oxygen
  5. antioxidant
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13
Q

Where are ROS most prevalent?

A

in blood and tissues as hydrogen peroxide

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14
Q

What types of molecules are antioxidants?

A

Vitamins A, C and E and uric acid

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15
Q

What does glutathione peroxidase do?

A

reduces lipid peroxides through oxidizing glutathione

- very important in ROS defense

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16
Q

What are some important properties of the liver?

A

central role of metabolism, filtration of ingested materials and excretory functions

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17
Q

What are some markers of mild liver disease?

A

typically no outward symptoms. Detected only as biochemical changes

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18
Q

What are some markers of severe liver disease?

A

yellow pigmentation, bruising readily, profuse bleeding, abdomen distended with fluid

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19
Q

What problems can liver disease lead to?

A

endocrine, CNS, skin, cardiovascular and GI problems

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20
Q

What are some special features of the liver?

A
  • structure facilitates exchange between hepatocytes and plasma
  • portal vein is found running through it
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21
Q

What plays a central role in glucose metabolism?

A

liver

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22
Q

How does the liver play a role in glucose metabolism?

A

Maintains circulating concentration of glucose

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23
Q

Why is the liver essential for glucose metabolism?

A
  1. kidneys do not store glycogen
  2. muscles store glycogen (more than the liver) but do not have glucose-6-phosphatase which allows glucose to be release into blood.
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24
Q

What are the liver plasma proteins?

A

albumin, coagulation factors, alpha and beta plasma globulins, acute phase proteins

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25
Q

What do acute phase proteins do?

A

C-reative proteins (proteins that measure general levels of inflammation in the blood) are released by damaged tissue or infective agents during actor phase response

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26
Q

Why is the urea cycle important?

A

removal of nitrogen generated by amino acid metabolism

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27
Q

What does catabolism of amino acids generate?

A

ammonia and ammonium ions (toxic to CNS)

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28
Q

How is ammonia detoxified?

A

on site by admiration of glutamate to glutamine

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29
Q

What happens to remaining nitrogen?

A

enters the portal vein as ammonia or alanine so the liver can convert the ammonia/ammonium to urea for excretion

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30
Q

What is heme?

A

O2 binding moiety common to Mb and Hb

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31
Q

Where does heme synthesis occur?

A

1st in the mitochondria, then the cytoplasm then back to the mitochondria

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32
Q

What is the rate limiting step during heme synthesis?

A

glycine and succinyl-coA condense to form 5-ALA. This reaction is synthesized by 5-ALA synthase in the mitochondria

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33
Q

T/F Heme controls its own synthesis

A

T; hemne inhibits 5-ALA synthase

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34
Q

What is bilirubin?

A

product of heme catabolism excreted in bile and urine

35
Q

What is jaundice?

A

when there is excess of plasma bilirubin as there is an imbalance between its production and secretion

36
Q

What are the three main causes of jaundice?

A

Prehaptic: increased production of bilirubin as a result of hemolysis
Intrahepatic: impaired hepatic uptake, conjugation or secretion of bilirubin
Posthepatic: obstruction to biliary drainage (in complete obstruction urobilinogen and urobilin are absent from urine)

37
Q

Is bilirubin soluble?

A

No, requires carrier protein; biliverdin is

38
Q

Where are drugs metabolized?

A
  • most in the liver
39
Q

How are drugs metabolized?

A

Phase I = addition of polar group mediated by cytochrome P-450
Phase II = conjugation mediated by cytoplasmic emzymes (sulfation, acetylation, methylation)

40
Q

What role does cytochrome P-450 play in drug metabolism?

A

active site contains a heme iron center that is important for oxidation of organic substances

41
Q

What happens when acetaminophen is taken in therapeutic doses?

A

it is conjugated to glucouronic acid and excreted

42
Q

What happens when acetaminophen is taken in excess?

A

produces free radical (causes toxicity), hepatotoxic in excess

43
Q

What is the most common cause of liver disease?

A

excess intake of alcohol

44
Q

Why is glucose critical?

A

fuels the brain and is preferred energy source in muscle

45
Q

What is the long-term energy storage of glucose?

A

glycogen

46
Q

Can AA be used as an energy source?

A

Yes, during fasting or metabolic stress. If excess are ingested in diet they are converted to carbs and stored

47
Q

What is plasma glucose concentration the result of?

A

intake, production and tissue utilization

48
Q

What types of cells produce insulin and glucagon?

A

insulin is secreted by beta cells and glucagon is secreted by alpha cells (both from pancreatic cells)

49
Q

What is the source of glucose in FED and starving states?

A

In fed state it is from the diet but in starved states it is from glycogen

50
Q

What are the phases of insulin production after oral glucose?

A

1st phase is from glucose stimulation, them by AA through stimulation of the vagus nerve and hormones secreted by the gut

51
Q

What are some effects of insulin?

A

promotes anabolism in the liver, adipose tissue and muscle

52
Q

What are the causes of type 2 diabetes?

A

insulin resistance and impaired insulin secretion

53
Q

What role does GLUT4 play with insulin in the cell?

A

insulin dependent glucose entry into the cell is mediated by glucose transporters (GLUT4)
- controls glucose uptake in skeletal muscle and adipocytes

54
Q

Where doe most GLUT4 molecules reside?

A

intracellularly

55
Q

Why does insulin double rescruitment of the transporter to the cell membrane in humans?

A
  • muscular contraction increases expression of GLUT4 independently of insulin
  • fatty acids decrease expression of GLUT4 in muscle
56
Q

What are the effects of insulin

A

promotes anabolism in the liver, adipose tissue and muscle

57
Q

What are main contributors of type 2 diabetes?

A

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

58
Q

What results from defects in insulin signaling?

A

receptor binding could be compromised, mutation in the insulin receptor gene or anti-receptor autoantibodies could be in effect

59
Q

What is the function of glucagon?

A

mobilizes glucose, increases blood glucose, stimulates catabolism, surpasses anabolsim

60
Q

What are the function of epinephrine in energy metabolism?

A

Secreted by adrenal gland, inhibits glycolysis, lipogenesis, stimulates gluconeogenesis

61
Q

What occurs during phosphorylation in catabolism?

A

glucagon stimulates activation of Fru-2,6-Bisphosphate causing decrease if Fru-2,6-BP which has a reciprocal inhibitory effect on mainline PFK1 inhibiting glycolysis

62
Q

What does glucagon action result in?

A

stimulation of gluconeogenesis and inhibition of glycolysis

63
Q

What does phosphorylation typically stimulate?

A

enzymes in catabolic pathways and inhibits anabolic ones

64
Q

What are causes of hypoglycemia?

A

exercise, fasting, excess endogenous and exogenous insulin, inhibition of glucose production

65
Q

What controls the Feed-fast cycle?

A

changes in plasma ratios of insulin and glucagon (ratios of insulin/glucagon)

66
Q

What are the significant ratios of insulin/glucagon?

A

after eating for several hours = insulin high/glucagon low
During fasting = glucagon his/insulin low
Starvation = low insulin and high glucagon

67
Q

What are the substrates for gluconeogenesis?

A

lactate, alanine, glycerol

68
Q

What is the cori cycle?

A

allows recycling of glucose back to lactate

69
Q

What is the major energy substrate during prolonged starvation?

A

free fatty acids

during starvation gluconeogenesis occurs in kidney and liver

70
Q

What anti-insulin hormones are secreted during stress metabolism?

A

epinephrine, glucagon, cortisol

71
Q

What is the response during stress?

A

decreased anabolism and increased catabolism

72
Q

What are the outcomes of the stress response?

A

induces insulin resistance, cortisol decreases GLU4
expression and induces expression of G6P
Glucose independent glu uptake increase

73
Q

What are the differences between type 1 and 2 diabetes?

A

type 1 is the destruction of beta cells while type 2 involves insulin resistance and impaired insulin secretion

74
Q

T/F Type one diabetes in not an inherited disease

A

F

75
Q

Who is prone to ketoacidosis and dependent on insulin?

A

diabetics

76
Q

What role does ketoacidosis play in type 1 diabetes?

A

ketone bodies accumulate in plasma increasing blood H+ and lowering blood pH = diabetic ketoacidosis
- major complication of poorly controlled diabetes

77
Q

Which type of diabetes is the result of obesity?

A

Type 2 but weight loss with exercise can often reverse it

78
Q

Which type of diabetes is macroangiopathy more prevalent in?

A

2

79
Q

What are the clinical symptoms of lack of insulin?

A

increased lipolysis -> increased ketogenesis -> acidosis -> compensatory hyperventilation
Increased gluconeogenesis -> hyperglycemia -> glycosuria + acidosis -> osmotic diuresis -> dehydration

80
Q

What are the vascular complications with diabetes?

A

Hyperglycemia leads to atherosclerosis, microangiopathy, cataracts and eye nerve conduction defects

81
Q

What is the glucose tolerance test?

A

add glucose to blood stream and monitor glucose cellular consumption

82
Q

What is the A1C test?

A

hemoglobin can be modified by glycation, more glucose in blood leads to more glycation on hemoglobin. Degree of glycation is an indicator of glucose exposure over RBC lifespan

83
Q

What are treatments for diabetes?

A

type 1 = diet, exercise, maintain blood glucose, use of insulin
type 2 = treat with oral hypoglycemic drugs(sulfonylureas and thiazolidineadiones)

Biochem Exam 3 (4 decks)

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