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P1 > BSI EXAM 3 > Flashcards

BSI EXAM 3 Flashcards

1
Q

Where does glycolysis take place?

A

cytosol

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2
Q

Where does Krebs cycle take place?

A

mitochondria

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3
Q

Where does ETC take place?

A

inner mitochondrial membrane

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4
Q

Where glycogenesis stored?

A

liver and muscle

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5
Q

Where does glyconeogenesis take place?

A

liver and kidneys

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6
Q

Where does glycogenolysis take place?

A

liver and muscle

Exception is glucose 6 phosphotase only happens in liver

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7
Q

What is the net ATP and net NADH from oxidation of glucose into pyruvate?

A

2ATP

2NADH

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8
Q

How many molecules of pyruvate do you end up with when partially oxidizing one molecule of glucose?

A

2

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9
Q

What are the rate limiting enzymes of glycolysis?

A

Hexokinase
phosphofructose kinase
pyruvate kinase

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10
Q

What is the function of NAD+ and FAD+?

A

to carry electrons

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11
Q

What are 3 conditions in which the conversion of pyruvate to lactate will increase?

A
  1. no oxygen
  2. mitochondria dysfunction
  3. pyruvate is accumulating faster than mitochondria
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12
Q

How is lactate handled by the body? (in other words, how is it removed?)

A

other cells and tissues that are better oxygenated can take up and use it for energy.

lactose oxidized back to pyruvate–> acetyl coA–> krebs cycle

In this case, cell with mitochondria will take advantage by making the lactate to convert to pyruvate and then enter to mitochondria

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13
Q

What is the definition of lactic acidosis?

A

build up of lactate

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14
Q

Is the build-up of lactate causing the acidosis?

A

no, acidosis is build up of protons

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15
Q

Name 4 molecules that will directly stimulate the rate of glycolysis.

A

ADP, Pi, insulin, epinephrine

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16
Q

Name 2 molecules that will directly inhibit or decrease the rate of glycolysis.

A

ATP, Glucogon

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17
Q

What enzyme catalyzes the conversion of pyruvate into acetyl-CoA? In this reaction, what is being oxidized and what is being reduced?

A

Pyruvate dehydrogenase= pyruvate+NAD + coA—> acetyl coA+ CO2+ NADH + H+

Pyruvate reduced
Acetyl coA oxidized

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18
Q

When completely oxidizing 1 molecule of glucose, how many molecules of acetyl-CoA will go through the Krebs Cycle?

A

2

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19
Q

How many ATP, NADH, and FADH2 do you get with one turn of the Krebs Cycle?

A

1ATP
3NADH
1FADH

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20
Q

What are the rate limiting enzymes of the Krebs Cycle? What molecules regulate their activity?

A
  1. Pyruvate dehydrogenase
  2. citrate synthase
  3. Isocitrate dehydrogenase
  4. alpha- ketoglutarate
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21
Q

Where in the cell does Krebs Cycle take place?

A

mitochondria

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22
Q

What does NADH and FADH2 do with their electrons they are carrying?

A

both carry 2H+ when oxidized

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23
Q

What is the path of electron flow through the ETC from NADH?

A

NADH: 1–> coQ–>3–> cyto c–> 4

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24
Q

What is the path of electron flow through the ETC from FADH2?

A

FADH: 2–>CoQ–>3–>cyto C–> 4

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25
Q

Why does the electrons coming from NADH produce 2.5 ATP?

A

10H+ pumped out and 4H+ required to make 1 ATP

10/4= 2.5ATP

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26
Q

Why does the electrons coming from FADH2 produce 1.5 ATP?

A

6H+ pumped out and 4H+ required to make 1 ATP

6/4= 1.5ATP

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27
Q

If there is lack of oxygen, why does the ETC shut down?

A

YES

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28
Q

If there is lack of oxygen, why does the Krebs Cycle shut down?

A

YES

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29
Q

If there is lack of oxygen, why does the glycolysis shut down?

A

Because mitochondria need oxygen to produce ATP. No ATP= no glycolysis

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30
Q

what happens in dihydroxyacetone phosphase?

A

it converted to glyceraldehyde 3 phosphate

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31
Q

what is the function of NAD+?

1) To carry oxygen to mitochondria
2) to carry electrons
3) its an enzyme and catalyze various rxn

A

2) to carry electorns

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32
Q

Pyruvate—–> lactate

Under what condition this happens?

A

1) lack of oxygen- only applies maxiumum level of intensity
2) catholigcal reason- mitochondria dysfunction- diease states that no produce proteins from mitochondria
3) pyruvate is accumumlating gaster than mitochondria- glycolysis and pyruvate exceeded the pathway

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33
Q

What rxn is pyruvate—> Lactate
what is the enzyme?
what is oxidized

A

reverse reaction
lactate dehydrogenase
NADH to NAD+

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34
Q

Lactic acidosis is a cause for muscle fatigue and “stingly” of the muscles during high intensity exercise
T or F?

A

T

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35
Q

Lactic acidosis is a cuase for delayed onset muscle soreness after exercise
T or F?

A

F; due to inflammation response

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36
Q

Pyruvate—> Krebs cycle oxidized

what is net NADH?

A

4

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37
Q

How many NADH produce with 1 acetyl coA?

A

3

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38
Q

How many net ATP, NADH, FADH2 in the process of completely oxidized krebs cycle?

A

4ATP
10NADH
2FADH2

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39
Q

How lack O2 stops ATP synthase?

A

electron flows= maintain proton gredients missing -> cant have ATP synthase

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40
Q

Damage mitochondria DNA, how does it lead to lactic acidosis?

A

mitochondrial dysfunction= proton is building up

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41
Q

How does mitochondria DNA damage cause mitochondrial dysfunction?

A

Remember 13 proteins in ETC
Dysfunction will shut dow ETC and lead to shut down in ATP and Krebs cycle
No mitochndria= no pyruvate= accumulate lactose instead of protons= going faster than its suppose to

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42
Q

What is the difference between glucokinase and hexokinase?

A 
glucokinase= in liver
hexokinase= not in liver
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43
Q

What effect does insulin and glucagon have on glycogenesis? Glycogenolysis?

A

increase glucogon

decrease insulin

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44
Q

Does glucagon affect glycogenesis and glycogenolysis in skeletal muscle? Liver?

A

liver

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45
Q

During a state of starvation, is glycogenesis in the liver stimulated or inhibited? What about the fed state?

A

Starvation: inhibit
Fed: stimulate

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46
Q

During a state of starvation, is glycogenolysis in the liver stimulated or inhibited? What about the fed state?

A

Starvation: stimulates
Fed: inhibit

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47
Q

Define gluconeogenesis. What substrates can be used for gluconeogenesis?

A 
Forming new glucose
aa
lactase
gylcerol
oaa
48
Q

For what purpose does the liver release glucose into the blood?

A

so brain can function

49
Q

Why don’t you become hypoglycemic in the middle of the night when you are sleeping and haven’t eaten in several hours? What happens to your insulin and glucagon levels in the middle of the night?

A

glycogenesis and glyconeogenesis is in the liver provides glucose to dump in to the blood

50
Q

What effect does insulin and glucagon have on gluconeogenesis?

A

Glycogenolysis
Stimulate glucogon
Inhibit insulin

Glycogenesis
Stimulate insulin
Inhibit glucagon

51
Q

What happens to gluconeogenesis right after you eat a meal (is it stimulated or inhibited)?

A

inhibit

52
Q

metformin decreases the activity of glucose 6 phosphate. what effect this have on the body?

1) it will inhibit glycolysis in all tissues
2) it will inhibit glycogenolysis in muscle tissue
3) it will inhibit glyconeogenesis in muscle
4) it will inhibit glyconeogenesis in the liver

A

4

53
Q

why skeletal muscle is not taking glucose?

A

insulin stimulate anabolic pathway
it stimulate uptake of glucose
since decreased in insulin, there is no insulin to uptake the glucose
brain does not insulin to take it up

54
Q

glycolysis: oxidized sugar

glucagon inhibits? stimulates?
insulin inhibits? stimulates?

A

glucagon inhibits

insulin stimulates

55
Q

glycogenesis: forming glycogen trees

glucagon inhibits? stimulates?
insulin inhibits? stimulates?

A

glucagon inhibits

insulin stimulates

56
Q

glycogenolysis: breaking down glycogen trees

glucagon inhibits? stimulates?
insulin inhibits? stimulates?

A

glucagon stimulates

insulin inhibits

57
Q

glyconeogenesis: forming new glucose and move along to blood

glucagon inhibits? stimulates?
insulin inhibits? stimulates?

A

glucagon stimulates

insulin inhibits

58
Q

lipolysis

glucagon inhibits? stimulates?
insulin inhibits? stimulates?

A

glucagon stimulates

insulin inhibits

59
Q

Lipogenesis

glucagon inhibits? stimulates?
insulin inhibits? stimulates?

A

glucagon inhibits

insulin stimulates

60
Q

ketogenesis

glucagon inhibits? stimulates?
insulin inhibits? stimulates?

A

glucagon stimulates

insulin inhibits

61
Q

krebs cycle

glucagon inhibits? stimulates?
insulin inhibits? stimulates?

A

glucagon inhibits

insulin stimulates

62
Q

b-oxidation

glucagon inhibits? stimulates?
insulin inhibits? stimulates?

A

glucagon stimulates

insulin inhibits

63
Q

why can’t the brain use fat for energy?

A
  1. neurons don’t express b-oxidation enzymes

2. free fatty acids bound to albumin cannot cross the blood-brain barrier

64
Q

why can’t fats used for energy under anaerobic conditions or any other condition that will shut dow the ETC?

A

if ETC shuts down, NADH and FADH2 cannot be recycled back to NAD+ and FAD+.
B-oxidation will shut dow—> fatty acid will never tranfer to the mitochondria matrix and will accumulate in cytosol.
same does to mitochondrial dysfunction

65
Q

B-oxidation is the process of cleave the bond between a fatty acid and glycerol backbone in the trigylceride molecule

T or F?

A

False; this is definition of lipolysis

B-oxidation is 4 steps process of cleaves off 2c from fatty acids coA in the form of acetyl coA

66
Q

Insulin increases phosphodiesterase activity in adipocytes. What effect this have on lipolysis

  1. stimulate lipolysis
  2. inhibit lipolysis
  3. no effect
A
  1. inhibit lipolysis

insulin stimulates anabolic and inhibits catabolic

Why?

incerased phosphodiesterase activity will decrease the amount of cAMP, therefore decrease activity of hormone sensitive lipase and decrease lipolysis

67
Q

What are the main functions of epithelial tissue?

A

protection, absorption, secretion, ion transport, filtration plus “slippery when wet.”

68
Q

Cillia do what?

A

propel stuff (eggs, sperm and mucus)

69
Q

Villi do what?

A

↑surface area (for absorption).

70
Q

Which of these cell types is considered to be connective tissue?

  • oesteoblasts
  • adipocytes
  • goblet cells
  • mast cells
  • RBC’s
A

all but Goblets.

71
Q

Fibroblasts secrete which fiber types?

A

all 3; collagen, elastic and reticular

72
Q

Dense irregular connective tissue cannot?

A

withstand ↑tension in one direction

73
Q

Dense regular connective tissue cannot?

A

withstand ↑tension in multiple directions.

74
Q

What type of connective tissue forms the vertebral discs?

A

fibrocartilage

75
Q

Is the statement “the terms dorsal and posterior are synonymous in four-legged animals” true or false?

A

false

76
Q

The elbow is more what relative to the wrist?

A

proximal

77
Q

A rostral to caudal brain section not along the midline is what type of section?

A

sagittal

78
Q

The thorax is what to the abdomen?

A

superior

79
Q

Are the serous membranes just to reduce friction of moving organs?

A

no, in the lungs they also link the alveoli to the thoracic wall

80
Q

Do the body’s systems try to maintain exact physiological values such as body temperature?

A

not an exact value but a narrow range depending on variable.

81
Q

Significant variations in all physiological parameters can be tolerated; true or false?

A

False; depends on variable- ↑BP can be tolerated for years but a significant change in body temperature or especially pH cannot.

82
Q

What is the normal mechanism for limiting change and restoring homeostasis?

A

negative feedback.

83
Q

Where is the best place to control metabolic pathways?

A

: at the first step/first enzyme.

84
Q

What is vital if utilizing positive feedback for physiological processes?

A

: to have a separate, limiting mechanism (not self-limiting like negative feedback).

85
Q

What are the 4 types of tissue? (histologically speaking).

A

epithelial, connective, muscle and nervous.

86
Q

Why do you need to stain tissues?

A

most tissue is colorless (Caucasians only really have a pink tinge due to blood!) so without the contrast afforded by specific dyes you would find it very difficult to discern anything down a microscope.

87
Q

Where did the first histological stains originate from? (developed from?).

A

the first stains were dyes used to stain material woven for clothes.

88
Q

What are the resolving limits of normal/light microscopy?

A

: about the size of a small bacterium (~1m to 100nm); limited by the wavelength of visible light.

89
Q

What are the main problems with normal/light microscopy?

A

in most situations the processing; impregnating the tissue with wax so it can be cut requires treatment with harsh chemicals, etc. Additionally, the microscope must be set up carefully (“critical illumination”) to get the correct stain colors especially for photography.

90
Q

What are the resolving limits of electron microscopy?

A

almost down to single atoms! (~0.1nm/electrons).

91
Q

What are the main problems with electron microscopy?

A

the processing even more so. Electron microscopy requires that the tissue be in a vacuum (where no one can hear you scream- see below!) and it is therefore totally dehydrated which is even more likely to introduce artifacts (something added by the experiment/observation/whatever which confounds your results and/or observations) than preparing tissue for light microscopy.

92
Q

mitochondrial dysfunction in the liver can cause ketoacidosis

T or F?

A

False; acetyl coa is produced in mitochondria so when mitochondria shut down at the acetyl coa will not formed. so cant synthisize ketone bodies
if mitochondria shut dow, then ketogensis cannot occur

93
Q

Anaerobic conditions can cause high rish of ketoacidosis

T or F?

A

False
anaerobic condition–> no o2–> etc shut down–> krebs cycle shut down–> cannot use fat because no b-oxidation and no ketoacidosis

94
Q

a common adverse side effect of Zidovudre is ketoacidosis

T or F?

A

False

95
Q

Lack of insulin and high secretion of glycogen is a common cause if ketoacidosis

T or F?

A

True

example= uncontrolled type 1 diabetes

96
Q

Ketosis

A

example= fasting, or eating high fat and low carb
high rate of b-oxidation and low krebs –> high glucagon and low insulu=in

common

97
Q

ketoacidosis

A

example= uncontrolled type 1 diabetes
very very very high level of b-oxidation
glucagon

high level of glucagon will attack bodies such as pancreases when it have “0” insulin

Because glucagon is high, glyconeogenesis is going to happen even though its not suppse to becasue we do not have insulin to uptake glucagon

OAA will deplet–> accumulation of acetyl coa

98
Q

Tolbutamine and glyburide (drugs to treat diabetes) can inhibit carnitine palmotoyl transferase 1 ( as a side effect) which leads to muscle weakness, pain and exercise intolerance. why would this cause exercise intolerance?

  1. they inhibit use of glucagon as a fuel source
  2. they inhibit use of blood glucose as fuel source
  3. they stimulate ketogenesis
  4. they inhibit use of fats as a fuel source.
A

4

why?
cannot transport fatty acids into the mitochondrial matrix for b-oxidation, so cannot use fats a fuel course which can lead to weakness and exercise intolerance
the pain is due to accumulation of lipid droplets in the cytosl of the cell. Accumulation fo lipids cell (except adipocytes) cause dyfunction or death of the cell

accumulations in cytosol are bad!!

99
Q

Zidovudine can deplete mitochondrial DNA. How can this lead to steatosis?
(accumulation of lipids in the cell)

A

Damage mitochondria–> no ETC
Depletion of mtDNA (low mtDNA) will lead to dysfunctional ETC and it will shut down. Therefore, B-oxidation will shut down. If B-oxidaiton shut down, then the fatty acids will not be transported into the mitochondria and will then accumulate in the cytosol. Steatosis can cause dyfunction or death to thecell
mtDNA does not encoded bust some of ETC

100
Q

What tissue does ketogenesis take place?

A

liver

101
Q

what are ketone bodeis made from?

A

acetyl coa

102
Q

what is ketoacidosis cause from?

A

accumulation of ketone bodies

103
Q

how are most of the ROS/RNS produced in the body of external source?

A

in the mitochondria of most cells via ETC

104
Q

what is Doxorubicin?

A

cause damage in health heart cell
cancer drug stimulate HO* to heard
increase H2O2 and increase irons to the heart

105
Q

What is Dexrazoxane?

A

prevent doxorubicin
when patient is given binds to free ions
ion is not free it can react
this helps reduce OH*

106
Q

4 main cell types of epidermis

A

Keratinocytes, melanocytes, Merkel cell, and langerhans cell

107
Q

Nailed are modified epithelial tissue composed of what?

A

Hard keratin

108
Q

First degree burn?
Second degree burn?
Third degree burn?

A 
First= only epidermis 
Second= epidermis and dermis 
Third= all
109
Q

Melanomas

A

Developed from moles

Arise from melanocytes

110
Q

Psoriasis

A

Due to excessive growth of keratinocytes and like eczema

It has inflammation

111
Q

Homeostasis

A

Dynamic mechanism that detect and response to deviations

112
Q

Afferent

A

Sensory information going in

113
Q

Efferent

A

Muscle response

114
Q

Example of positive effect

A

Blood clots and child birth

Positive effect is non self limited

115
Q

Example of negative feedback

A

Alosteric modulators

Negative feedback is self limiting

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