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Human Form and Funciton > Quiz 6 > Flashcards

Quiz 6 Flashcards

1
Q

What are the four phases of the male excitatory response? What nerve controls each one?

A

Stimulation: pudendal (somatic)

Erection: Pelvic splanchnic (parasympathetics)

Emission: Lumbar and sacral splanchnic (sympathetics)

Ejaculation: Pudendal nerve (somatic)

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2
Q

The pudendal nerve arises from where in the spinal cord?

A

S2-S4

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3
Q

The parasympathetics that cause erection arise from where?

A

Lateral horns of s2-s4.

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4
Q

The pelvic splanchnic nerves go through what plexi?

A

Pre-aortic and prostatic plexus

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5
Q

What causes vasodilation of the deep penile arteries? This causes blood to fill what erectile tissue?

A

NO

Corpus and spongy cavernousum

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6
Q

The pre-aortic plexus is also known as the…

A

Inferior hypogastric plexus

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7
Q

The urethra goes through what structure in the penis?

A

Corpus spongiosum

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8
Q

What is the only structure superficial to the deep penile fascia?

A

Superficial dorsal vein

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9
Q

The dilation of the corpus cavernousum causes what vein to pinch off?

A

Deep dorsal penile vein

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10
Q

The sympathetics that result in emission come from where?

A

Lateral horns of T10-L2

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11
Q

The lumbar and Sacral splanchnic nerves go to what plexi?

A

Inferior hypogastric plexus.. Which then go to the spermatic tubes

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12
Q

What does norepinephrine do in the male excitatory response?

A

Causes peristaltic contractions of the ductus deferens, seminal vesicles, prostatic smooth muscles, and constriction of internal urethral sphincter

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13
Q

The closing off of the urethral sphincter serves what purpose in the male excitatory response?

A

Prevents back flow into the bladder

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14
Q

In the ejaculation phase, what muscles are stimulated by the pudendal nerve to contract?

A

Bulbospongiosus and ischiocavernosus muscles contract

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15
Q

What 2 organs regulate metabolism?

A

Pancreas and Liver

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16
Q

What cells of the pancreas secrete insulin and glycogen?

A

Islet cells

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17
Q

What are the key regulators of metabolism?

A

Insulin, glucagon, epinephrine, glucose, ATP/AMP

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18
Q

What are the four fates for glucose?

A

Pyruvate (glycolysis)

Ribose 5 phosphate (pentose phosphate pathway)

Glycogen/starch (storage)

Synthesis of structural polysaccharides

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19
Q

Glycolysis and gluconeogenesis, glycogenesis and glycogenolysis, are exclusive. What does this mean?

A

Only one or the other can be performed in a cell at a time.

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20
Q

Gluconeogenesis can occur in all cells, but where does it primarily take place?

A

Liver

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21
Q

Where is excess glucose stored?

A

Liver or adipose. If not glycogen

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22
Q

What cells would contain the most glycogen?

A

Liver and muscle cells

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23
Q

How does glycogen play a role in osmolarity?

A

400 glucose molecules compared to 1 glycogen molecule. Less molecules = less concentrated solution.

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24
Q

Why is putting phosphates on glucose important?

A

It prevents the glucose from leaving the cell and allows energy to be transferred and used later

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25
Q

What enzyme is the point of regulation in glycogenesis?

A

Glycogen synthase

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26
Q

Does glycogen synthase add new UDP-glucose to the reducing or non reducing end?

A

Non reducing end

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27
Q

Glycogen phosphorylase. What is it? What end does it work on?

A

Removes glucose 1 phosphate molecules from glycogen from the non reducing end

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28
Q

Where would you find glucose-6-phosphatase?

A

Only in the liver (in the ER) It dephosphorylates glucose-6-phosphate so that the glucose molecules can exit the cell and into the bloodstream. Thus increasing blood sugar levels.

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29
Q

Glycogen synthase is activated by what factors?

A

Insulin, glucose 6 phosphate, glucose. Insulin also causes the inhibition of the deactivation of glycogen synthase a (active form)

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30
Q

What will prevent the activation of glycogen synthase?

A

Glucagon/epinephrine

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31
Q

Glycogen is allosterically regulated by… … Does this activate or deactivate glycogen synthase?

A

Phosphate. 3 phosphates deactivate glycogen synthase.

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32
Q

How does insulin prevent the deactivation of glycogen synthase?

A

Insulin inhibits glycogen synthase kinase 3.

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33
Q

Glycogen phosphorylase. Which is active, the phosphorylated or non phosphorylated form? What about glycogen synthase?

A

Glycogen phosphorylase is active when it is phosphorylated.

Oppositely, glycogen synthase is inactive in its phosphorylated form

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34
Q

What causes the activation of glycogen phosphorylase?

A

Glucagon, epinephrine

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35
Q

What are some things insulin does?

A

Activates GLUTs, hexokinase, glycogen synthase.

Also, it deactivates glycogen synthase kinase.

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36
Q

True or false… Glucagon and Epinephrine act on both liver and muscle cells.

A

False. Epinephrine acts on both but glucagon only acts on liver cells

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37
Q

What happens to the liver when it is affected by glucagon?

A

Glycogenolysis increases
Glycolysis decreases
Gluconeogenesis increase

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38
Q

What happens to muscle cells when they are affected by epinephrine?

A

Glycogenolysis increases

Glycolysis increases

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39
Q

What is the input cost to produce one glucose molecule via the cori cycle?

A

4 ATP
2GTP
2 NADH

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40
Q

Where is the point of regulation in glycolysis and Gluconeogenesis?

A

Enzyme phosphofructokinase-1 (glycolysis)

Enzyme
Fructose 1-6 bisphosphatase - 1
Gluconeogenesis

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41
Q

How is phosphofructokinase 1 and fructose 1,6 bisphosphatase 1 regulated?

A

ADP and AMP will stimulate phosphofructokinase -1 to allow glycolysis to go. (AMP will also inhibit fructose 1,6 bisphosphatase1)

ATP and Citrate will inhibit phosphofructokinase 1 to prevent glycolysis from occurring.

42
Q

What is AMPK?

A

Kinase that detects levels of intracellular levels of AMP. This will cause systemic changes such as less insulin secretion, less fatty acid synthesis, more fatty acid uptake in muscles and heart.

43
Q

Electrons are being moved from glucose to other molecules. Thus glucose is being ____ while the other molecule is being _____

A

1) oxidized

2) reduced

44
Q

The preparatory phase of glycolysis is ____ while the payoff phase is ___.

A

1) phosphorylation

2) REDOX

45
Q

Fermentation is defined as…

A

The build up of NADH. Which must be restored back to NAD+

46
Q

Cancer cells have a higher or lower rate of glycolysis?

A

Higher.

47
Q

When does the glycolysis preparatory phase end?

A

Once glyceraldehyde 3 phosphate is formed

48
Q

True or false… All dietary carbohydrates are converted into glucose before glycolysis?

A

False. Some directly feed into glycolysis at different steps

49
Q

What are the three fates of glucose?

A

Stored as glycogen
Converted to pyruvate (glycolysis)
Can enter the pentose phosphate pathway.

50
Q

What is the pentose phosphate pathway? What does it produce?

A

It produces NADPH.

turns glucose into ribose 5- phosphate (precursor for nucleotides, coenzymes)

51
Q

What is NADPH? Functions?

A

It is necessary for reductive biosynthesis (creating fatty acids)

Free radical protection

52
Q

How is the pentose phosphate pathway regulated?

A

Negative feedback.

Excess NADPH will shut off the pentose phosphate pathway

53
Q

What is the electron acceptor for fermentation in humans?

A

Lactate

54
Q

Where is lactate sent to be converted back to glucose?

A

The liver (Gluconeogenesis)

55
Q

How are mitochondria involved in apoptosis?

A

Cytochrome C is located in the intermembrane space. When the permeability of the mitochondria increases, cytochrome C is released to cytosol.

56
Q

How is cytochrome C involved in apoptosis (programmed cell death)?

A

Cytochrome C will activate Caspases which cause the cell to start destroying their own components.

First forms an apoptosome, activates caspase dimers, these in turn activate other caspases.

57
Q

Is pyruvate actively or passively transported from the cytoplasm to the matrix of mitochondria?

A

Actively

58
Q

5 vitamins are needed for pyruvate dehydrogenase complex to work. What are these?

A

Pantothenic acid
TPP
Lipoate
Uhhh that’s all I know!

Pyruvate is added to acetyl coA

59
Q

Where is pyruvate added to coenzyme A to form acetyl coA?

A

Matrix of mitochondria

60
Q

Why will the citric acid cycle halt in the absence of oxygen?

A

Due to the buildup of NADH and FADH2

61
Q

The intermediate steps in the citric acid cycle are precursors for what?

A

Amino acids, lipids, etc.

62
Q

Glycolysis and CAC are allosterically regulated by what?

A

The products themselves. (ATP, NADH). Excess ATP and NADH will shut it off while AMP and ADP and NAD+ will turn it on

63
Q

Alpha ketogluterate is a precursor for what? Which in turn is a precursor what?

A

Glutamate. This is a precursor for purines and amino acids such as glutamine, proline, arginine.

64
Q

Citrate can be converted into…

A

Fatty acids and sterols

65
Q

Oxaloacetate is a precursor what? Which is a precursor for what?

A

Precursor for phosphopenolpyruvate. This is produced in the matrix of the mitochonrida but must be moved out of the mitochondria for it to be turned into… Amino acids or back to glucose

Oxaloacetate is also a precursor for other amino acids such as asparagine, which is a precursor for pyramidines

66
Q

Where can pyruvate enter the citric acid cycle? 2 ways. What enzyme?

A

Either attached to co enzyme A to become acetyl coA (normal way)

Orrrrr pyruvate can be converted to malate by malic enzyme.

67
Q

Succinyl coA is a precursor for what?

A

Porphyrins and Hemes

68
Q

In the electron transport chain… All complexes pump out hydrogen besides which complex?

A

Complex 2

69
Q

What is significant about complex 2. What is its name?

A

Succinate dehydrogenase. It is also part of the citric acid cycle. Turns succinate into fumerate. This is where FADH2 is produced.

70
Q

What complex is NADH added to? What about FADH2

A

Complex 1.

FADH2 = complex 2

71
Q

What is the role of cytochrome C in the electron transport chain?

A

It is an electron carrier from 3 to 4

72
Q

Where is ubiquninone found? What does it do?

A

It’s found within the membrane of the electron transport chain because it is lipid soluble and membrane mobile.

It carries electrons and protons between the complexes

73
Q

True or false, fatty acids can enter the electron transport chain?

A

True

74
Q

Where does complex 3 transfer its electrons?

A

To cytochrome c

75
Q

How many ATP per NADH? What about FADH2?

A

NADH: 2.5 ATP
FADH2: 1.5 ATP

76
Q

How is ATP moved out of mitochondria?

A

Adenine nucleotide translocase (anti porter)

Brings ADP in (down conc. Gradient) and ATP out (against conc. Gradient)

Moves out of inner membrane space by porins

77
Q

What layer of the mitochonrida is impermeable to NADH?

A

Inner membrane

78
Q

What is the malate-aspartate shuttle? Where is it located?

A

The malate aspartate shuttle is located in the liver, kidney, and heart. It functions to bring NADH from glycolysis into the matrix of the mitochondria. NADH attaches to oxaloacetate to form malate, which is transported into the matrix via malate-alpha ketogluterate transporter. Aspartate exits the matrix via glutamate aspartate transporter. This turns into oxaloacetate to allow this whole process to occur again

79
Q

What is the glycerol-3-phosphate shuttle? Where is it located? Is it less effeciant or more efficient than the malate-aspartate shuttle?

A

Located in brain and skeletal muscle tissue. Less efficient than the malate-aspartate shuttle. Basically, the energy from NADH goes to FADH2

80
Q

What causes the build up of reactive oxygen species?

A

Mitochondria not making ATP. Lack of O2/ lack of ADP. The buildup of reduced quinone will transfer its electrons to oxygen to early to form ROS. Also the build up of NADH can cause ROS

81
Q

On the electron transport chain.. Where does the final electron acceptor accept electrons? Where is ATP produced?

A

O2 accepts electrons at complex 4. ATP is produced at ATP synthase

82
Q

What inhibits hexokinase?

A

Glucose 6 phosphate

83
Q

What activates the electron transport chain?

A

ADP. Thus the lack of ADP slows it down

84
Q

What bones make up the neurocranium?

A

Frontal, sphenoid (excluding the pterygoid process), temporal (only the squamous and petrous parts), pareital, occipital, ethmoid (only the cribriform plate)

85
Q

What is neurocranium vs viscerocranium

A

Neurocranium - bones that cradle the brain.

Viscerocranium - bones of the face. House sensory organs.

86
Q

What is Desmocranium vs chondrocranium?

A

Desmocranium - top portion of the neurocranium… Directly ossifies

Chondrocranium - base portion of the neurocranium….develops from a cartilaginous state

87
Q

Which bone makes up the superior portion of the orbit?

A

Frontal bone

88
Q

What kind of joint are the sutures in the skull?

A

Synarthroses

89
Q

True or false… The parietal bone is a weak part of the skull, prone to fracture.

A

False. The temporal bone is the weak point

90
Q

The squamous suture separates what two bones?

A

Parietal and temporal

91
Q

What bone(s) make up the anterior cranial fossa?

A

Frontal and sphenoid. And ethmoid

92
Q

What bone(s) make up the medial cranial fossa?

A

Temporal

93
Q

What is craniosynostosis?

A

Premature closure of sutures. Causes Brain to distort head shape. Serious cognitive defects

94
Q

What embryonic feature forms the vicerocranium?

A

Neural crest cells

95
Q

How many sinuses are in the skull? Name them

A 
4...
Frontal sinus
Ethmoid cells (sinuses) 
Maxillary sinus 
Sphenoid sinus
96
Q

Do sinuses get larger or smaller as we age?

A

Larger

97
Q

True or false… All sinuses are connected to the nasal cavity

A

True

98
Q

What is the strongest bone in the face?

A

Mandible

99
Q

What bones make up the orbit?

A

Frontal, zygomatic, maxillary, sphenoid, ethmoid, palatine, lacrimal

100
Q

What bones does the sphenoid bone touch?

A

Frontal, parietal, ethmoid, temporal, zygomatic, palatine, vomer, occipital

101
Q

What bone is the inferior nasal concha a part of?

A

Maxilla

102
Q

What sinuses drain into the middle meatus?

A

Frontal sinus, maxillary sinus, anterior ethmoid cells, middle ethmoid cells.

Human Form and Funciton (15 decks)

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