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Pathophysiology > Cells and Tissue Function > Flashcards

Cells and Tissue Function Flashcards

1
Q

The ribosomes on the rough ER have

A

a strand of mRNA attached to them

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2
Q

The protein that the rough ER ribosomes synthesize are destined to be part of

A

the cell membrane or the creation of lysosomal enzymes

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3
Q

The smooth ER does not

A

synthesize proteins

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4
Q

The smooth ER syntehsizes

A

lipids, steroids

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5
Q

The Smooth ER is also involved with

A

detoxification and the regulation of intracellular calcium

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6
Q

The sarcoplasmic reticulum of cardiac and skeletal muscle is a form of

A

smooth ER

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7
Q

The smooth ER of the liver is involved in

A

glycogen storage and the metabolism of lipid soluble drugs

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8
Q

What does the Golgi Apparatus do

A

modifies substances transfered from the ER

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9
Q

All lysosomal enzymes are

A

acid hydrolases

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10
Q

lysosomes maintain a internal pH of

A

5.0

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11
Q

What is the appx. pH of the cytosol and other organelles

A

7.2

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12
Q

What are lysosomes made from

A

digestive vesicles called endosomes

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13
Q

What is the first step in the creation of lysosomes

A

multiple endosomes form together to create an early endosome

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14
Q

The early endosomes turn into late endosomes as they

A

recycle lipids, proteins, and other membrane components back to the plasma membrane

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15
Q

What do the early endosomes uses to recycle the membrane components

A

recycling vesicles

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16
Q

The late endosomes mature into lysosomes as they

A

collect lysosomal enzymes

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17
Q

How do the late endosomes get their enzymes?

A

the enzymes are produced in the rough ER, sent and packaged in the Golgi Apparatus, then sent to the late endosome

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18
Q

How is a autophagosome formed

A

the ER isolated these particles from the cytoplasmic matrix by engulfing it in ER membranes

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19
Q

What is a autophagolysosome

A

when a lysosome and autophagosome fuse together

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20
Q

What are materials that remain undigested in the lysosome called

A

residual bodies

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21
Q

What are some examples of residual bodies

A

lipofuscin granules in neurons and heart muscle cells, inhaled carbon, and tattoo pigment

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22
Q

Lysosomes can also be repositories where

A

accumulate abnoramal substances

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23
Q

What type of disease is Tay-Sachs disease

A

lysosomal storage disease

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24
Q

What happens in Tay-Sachs disease

A

it is an autosomal recessive disorder where hexosaminidase A, needed to digest GM2 ganglioside is missing. as a result GM2 ganglioside accumulates in tissues like the heart liver spleen but it causes the most damage to the nervous system and retina.

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25
Q

The complex shape that DNA is coiled into is called

A

chromatin

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26
Q

Each complex of DNA and a histone protein is called

A

nucleosome

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27
Q

Because DNA is coiled too tight in the chromatin, it needs to be induced to change shape so it is accessable. What is this called

A

chromatin remodeling

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28
Q

Only mutations in ______ cells can be inheirited

A

germ cells

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29
Q

What kind of enzyme repairs DNA

A

endonucleases

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30
Q

After the endonucleases cleaves the distorted part of the DNA, what creates a new piece to put back

A

DNA polymerase

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31
Q

What binds the newly synthesized piece to the old strand

A

DNA ligase

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32
Q

Besides the nucleus, where is DNA stored

A

the mitochondria

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33
Q

Mitochondrial DNA is inheirited by who

A

the mother

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34
Q

What is its structure

A

single stranded closed circle

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35
Q

What are three differences of RNA from DNA

A

single stranded vs double
the sugar on the nucleotides are ribose not deoxyribose
thymine is replaced with uracil

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36
Q

What are the principal leukocytes of acute imflammation

A

neutrophils

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37
Q

What are the principal leukocytes of chronic infection

A

macrophages, lymphocytes, eosinophils, and mast cells

38
Q

How are endothelial cells involved in the imflammatory response?

A

They provide a semipermeable barrier for self and non-self, regulate leukocyte extravasation, release imflammatory mediators, and regulate immune cell proliferation by secreting hematopoietic colony-stimulating factors (CSF’s)

39
Q

What do endothelial cells also participate in

A

the repair process that follows imflammation by producing growth factors for angiogenesis and extracellular matrix synthesis.

40
Q

What leukocyte is arrives at the site of acute inflammation within 90 mins of injury

A

neutrophils

41
Q

What method do neutrophils use to kill pathogens

A

phagocytosis

42
Q

Besides its enzymes, what do neutrophils produce to aid in killing engulfed pathogens

A

they have oxygen-dependent metabolic pathways that generate toxic oxygen like hydorgen peroxide and nitric oxide

43
Q

How do neutrophils die

A

apoptosis

44
Q

How long does it take for neutrophils to dissappear after entering the site of inflammation

A

24-48 hours

45
Q

What percentage are eosinophils

A

2-3

46
Q

How long does it generally take for eosinophils to reach the site of inflammation

A

2-3 hours after the neutrophils

47
Q

Why do eosinophils take longer to reach the site of inflammation

A

they have slower mobility and slower reaction to chemotactic stimuli

48
Q

Inflammation is characterized as the

A

movement of fluid and leukocyte from vascular compartments into the extravascular tissue space

49
Q

Acute inflammation is characterized by the

A

exudation of fluid and plasma proteins

50
Q

Chronic inflammation is characterized by

A

angiogenesis, tissue necrosis, and fibrosis (scarring)

51
Q

What is the first phase of acute inflammation and what happens

A

during the vascular phase the blood vessels momentarily constrict then rapidly dilate, and permeability increases and protein rich fluid pours into the extravascular space.

52
Q

During the first phase of acute inflammation, what causes the cardinal signs like heat and redness

A

increased blood flow

53
Q

What cause the swelling and pain during the first phase of acute inflammation

A

increased osmotic pressure in the extravascular space coupled with an increase in capillary pressure cause the outflow of fluid

54
Q

How is the outflow and accumulation of fluid during the first phase of the acute inflammatory response beneficial

A

it helps localize any infectious pathogens

55
Q

What is the second phase of acute inflammation

A

during the cellular phase leukocytes are moved to the site of injury

56
Q

How is the second phase of acute inflammation broken down

A

margination, adhesion and trans migration, and chemotaxis

57
Q

What is margination

A

free flowing leukocytes leave the central blood stream and interact with endothelial cells

58
Q

What facilitates the adhesion and transmigration of leukocytes into the extravascular space

A

complemetary adhesion molecules like selectins and integrins

59
Q

What is the process of the third phase of acute inflammation

A

Opsonization: complement factor C3b and antibodies facilitates recognition of the neutrophil by the C3b receptor and Fc antibody receptor
Intracellular signal and actin essembly: Activation triggers intracellular siganling and actin essembly, forming pseudopods to enclose the microbe within a phagosome.
Formation of phagolysosome and killing: the phagosome fuses with a lysosome and then uses the enzymes and oxygen radicals to kill the microbe.

60
Q

Where are plasma derived mediators created

A

the liver

61
Q

Plasma derived mediators are products of three major protein cascade systems called

A

kallikrein-kininogen
the coagulation system
the complement system

62
Q

How do plasma derived proteins contribute to the inflammatory response

A

they cause vasodilation
increase vascular permeability
promote leukocyte adhesion, and chemotaxis
augment phagosytosis

63
Q

Where are plasma derived mediators created

A

the liver

64
Q

Plasma derived mediators are products of three major protein cascade systems called

A

kallikrein-kininogen
the coagulation system
the complement system

65
Q

How do plasma derived proteins contribute to the inflammatory response

A

they cause vasodilation
increase vascular permeability
promote leukocyte adhesion, and chemotaxis
augment phagosytosis

66
Q

What produce cell derived inflammatory mediators

A

tissue macrophages, mast cells, endothelial cells, platelets and leukocytes

67
Q

Histamine and serotonin are clasified as

A

vasoactive amines

68
Q

Histamine is derived from

A

histidine

69
Q

Serotonin is derived from

A

tryptamine

70
Q

What cell has the largest storage of histamine

A

mast cells adjacent to blood vessels

71
Q

What does histamine do

A

its causes dilation of arterioles and increases permeability of venules by binding to the H1 receptor of endothelial cells

72
Q

Where is serotonin primarily found

A

platelet granules

73
Q

Arachidonic acid is found where

A

the phospholipids of the cell membrane

74
Q

The release of what leads to the production of the eicosanoid family of inflammatory mediators

A

Arachidonic acid

75
Q

What are some inflammatory mediators are in the eicosanoid family

A

prostaglandins and leukotrienes

76
Q

Which two pathways does eicosanoid synthesis follow

A

cylcooxygenase pathway and lipoxygenase pathway

77
Q

Which synthesis pathway creates prostaglandins

A

cylcooxygenase

78
Q

Which synthesis pathway creates leukotrienes

A

lipoxygenase

79
Q

How do antihistames work

A

they act to competetively antagonize the h1 receptors by binding to them instead of histamine

80
Q

Which family of drugs blocks the inflammatory efffect of both the cyclooxygenase and lipoxygenase pathways

A

corticosteroids

81
Q

How do corticosteroids block the inflammatory efffect of both the cylcooxygenase and lipoxygenase pathways

A

they inhibit phosphodiesterase thus preventing the release of arachidonic acid

82
Q

Which prostaglandins induce inflammation and potentiate the effects of histamine and other mediators

A

PGD2, PGE2, PGF2alpha, PGI2

83
Q

Which prostaglandin promotes platelet aggregation and vasoconstriction

A

Thromboxane A2

84
Q

Which drugs effect the cyclooxygenase pathways

A

Aspirin and the NSAIDs

85
Q

What does NSAID stand for

A

nonsteroidal anti-inflammatory drugs

86
Q

How does aspirin and NSAIDs work

A

thhey inhibit the first enzyme in the cyclooxygenase pathway

87
Q

Leukootrienes have a similar function to

A

histamine

88
Q

Leukotrienes have been reported to affect the

A

permeability of venules,
adhesion properties of endothelial cells
and extravasation and chemotaxis of neutrophils, eosinophils, and monocytes

89
Q

Leukotreine LTC4, LTD4, and LTE4 cause

A

slow and sustained constirction of the bronchioles

90
Q

LTC4, LTD4, LTE4 are important inflammatory mediators in what conditions

A

bronchial asthma and anaphylaxis

Pathophysiology (91 decks)

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