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From Flashcardlet > Patho 1 > Flashcards

Patho 1 Flashcards

1
Q

What do all cells arise from?

A

Zygote

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2
Q

What is inflammation?

A

The body’s composite cellular reaction to injury

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3
Q

What is repair?

A

The process of healing the injury by regenerating new cells to replace dead ones or by filling the void and closing the wound with scar tissue

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4
Q

What is mitosis?

A

A process of organizing and dividing the nucleus into two daughter nuclei

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5
Q

What is a stem cell?

A

An unspecialized cell that in one mitotic cycle reproduces a copy of itself and creates a second, specialized cell

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6
Q

How are stem cells classified?

A

According to their power, or potency, codevelop into specialized cells

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7
Q

What are totipotent stem cells?

A

Most potent cells with the broadest powers to I’ve rise to an entire organism or to any particular type of cell in the body

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8
Q

What is an example of a totipotent cell?

A

Zygote

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9
Q

What is a pluripotent stem cell?

A

Subsequent stem cell generations beyond the initial eight stem cells become more specialized and less broadly potent - each differentiates into a more specialized version.
Can form any type of tissue but cannot form an entire human being

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10
Q

What is another name for pluripotent stem cells?

A

Embryonic stem cells

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11
Q

What is a multi potent stem cell?

A

As division continues and pluripotent cells differentiate into less potent, more specialized cells. Can produce a limited range of cell types

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12
Q

What are some examples of multi potent stem cells?

A

Mesenchymal stem cells - produce muscle, bone, ligament, or fat cells
Hematopoietic stem cells - produce blood and bone marrow cells

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13
Q

What are the two phases of the cell cycle?

A

Interphase and mitosis

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14
Q

What are the phases of the interphase?

A

G1, S, G2

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15
Q

What are the phases of mitosis?

A
  • Prophase
  • Metaphase
  • Anaphase
  • Telophase
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16
Q

What happens during prophase?

A

Nuclear membrane dissolves, and DNA organizes into dividing chromosomes (chromatids)

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17
Q

What happens during metaphase?

A

Chromatids align in the equatorial plane

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18
Q

What happens during anaphase?

A

Chromatids separate into new chromosomes

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19
Q

What happens during telophase?

A

Chromosomes uncoil and gather inside new nuclear envelope

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20
Q

What is the Ectoderm?

A

Differentiates into:

  • hair, nails, and epidermis (superficial layer of skin)
  • Brain
  • Nerves
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21
Q

What is the endoderm?

A

Differentiates into:

  • Internal lining of the intestinal and respiratory tracts
  • Liver
  • Pancreas
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22
Q

What is the mesoderm?

A

Differentiates into:

  • Deep layer of skin
  • Bone
  • Skeletal muscle
  • Blood vessels
  • Smooth muscle
  • Pleura
  • Peritoneum
  • Pericardium
  • Kidneys
  • Gonads
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23
Q

What does maintenance of life require?

A

Replacement of injured or dead cells with new cells

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24
Q

How do the cytoplasm and nucleus get divided in mitosis?

A

Half the cytoplasm is donated to each daughter, but nucleus copies into two

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25
Q

What three tissues does the zygote differentiate into?

A
  • Ectoderm
  • Endoderm
  • Mesoderm
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26
Q

What is the clinical application of adults having limited amounts of stem cells?

A

Scarring

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27
Q

What is produced after the replication of a stem cell?

A

A copy of the stem cell and a differentiated cell

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28
Q

What is a labile tissue?

A

Tissues that have many cells in the cell cycle at any given moment; cells divide frequently

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29
Q

Why do labile tissues divide constantly?

A

They are in need of ongoing replenishment because of constant damage or environmental exposure

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30
Q

What are some examples of labile tissues?

A
  • Skin
  • Urinary tract
  • Gi tract
  • Bone marrow
  • Bronchial epithelium
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31
Q

How do labile tissues repair?

A

Regeneration and/or fibrous repair (scarring)

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32
Q

What are stabile tissues?

A

Tissues that have only a few cells in the cell cycle at any given moment; cells do not divide frequently

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33
Q

When do stabile cells start dividing?

A

Although there are few cells in the cell cycle, they can ramp up proliferation a t a moment’s notice in response to a stimulus, like injury

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34
Q

What are some examples of stabile tissues?

A
  • Liver
  • Pancreas
  • Kidney
  • Smooth muscle cells
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35
Q

How do stabile tissues repair?

A

Regeneration and/or fibrous repair (scarring)

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36
Q

What are permanent tissues?

A

Tissues have very few or no cells in the cell cycle because they have very few or no stems cells

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37
Q

What are some examples of permanent tissues?

A
  • Brain
  • Skeletal muscle
  • Cardiac muscle
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38
Q

How do permanent tissues repair?

A

They cannot grow new tissue - fibrous repair (scarring) only
(Some instances of limited stem cell replacement)

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39
Q

What phase of the cell cycle are permanent tissues in?

A

G0

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40
Q

What phase of the cell cycle are labile and stabile tissues in?

A

G1

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41
Q

What is G0 phase?

A

“Resting phase” is a period in the cell cycle in which cells exist in a quiescent state, where the cell is neither dividing nor preparing to divide

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42
Q

What is G1 phase?

A

Cells increase in size in Gap 1, produce RNA and synthesize protein. G1 Checkpoint ensures that everything is ready for DNA synthesis

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43
Q

What is S phase?

A

To produce two similar daughter cells, the complete DNA instructions in the cell must be duplicated. DNA replication occurs during this S (synthesis) phase.

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44
Q

What is G2 phase?

A

During the gap between DNA synthesis and mitosis, the cell will continue to grow and produce new proteins. G2 Checkpoint determines if the cell can now proceed to enter M (mitosis) and divide. -

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45
Q

What is protooncogenes?

A

A hormone that promotes and stimulates cell growth

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46
Q

What are tumor suppressor genes?

A

They suppress the mitotic cycle

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47
Q

What is an example of a tumor suppressor gene?

A

P53

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48
Q

What does damage to the P53 gene cause?

A

Uncontrollable cell growth (cancer) because the body is unable to suppress the mitotic cycle

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49
Q

Why would an injury turn on a tumor suppressor gene?

A

Because the cells could stay in the G1 and S phase and rapidly prepare to divide, allowing cells to repair the tissue damage

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50
Q

How can cells be injured?

A
  • Anoxia, hypoxia, ischemia
  • Physical (chemical, radiation, toxins, microbes, inflammation and immune reactions, nutritions, genetic/metabolic, aging)
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51
Q

Can cell injury reverse?

A

Yes, in mild injury or stress

Severe injury or stress causes irreversible cell death

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52
Q

What happens to a cell if it can’t repair the damage?

A

Apoptosis - the cell destroys itself

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53
Q

How does lack of oxygen injure cells?

A

Without oxygen, cells cannot generate energy and therefore die

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54
Q

How do physical, thermal, or chemical agents injure cells?

A

Disrupt the structure of organs or tissues

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55
Q

How does radiation injure cells?

A

Ionizing radiation breaks water into hydrogen and hydroxyl ions. Hydroxyl ion attaches to DNA and prevents cell reproduction
Chronic radiation can cause DNA mutations that result in neoplasia

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56
Q

How do microbes injure cells?

A

Microbes can produce toxins that interfere with cell protein synthesis or cell oxygen utilization

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57
Q

How do inflammation and immune responses injure cells?

A

Reactions can release digestive enzymes deigned to neutralize foreign agents, but they can also digest healthy tissue
Also, autoimmune diseases

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58
Q

What is hydropic change?

A

Increased intracellular water, due to a change in the intracellular sodium concentration

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59
Q

Why does hydropic change occur?

A

Lack of oxygen deprives the NaK pump of energy, damaging the mechanism and allowing sodium to seep across the membrane, attracting water into the cytoplasm as well

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60
Q

Which process stimulates inflammatory response, apoptosis or necrosis?

A

Necrosis - cells can either adapt or die

Apoptosis is normal physiologic cell death, so it doesn’t cause an inflammatory response

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61
Q

What is steatosis?

A

Mild acute injury causes an accumulation of fat

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62
Q

Where is steatosis common?

A

Liver cells, because of the liver’s premier role in fat metabolism

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63
Q

What kind of patients present with steatosis?

A

Alcoholics, people with obesity

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64
Q

Is steatosis reversible?

A

Yes, if the causing agent is removed (if alcoholic continues to drink, may lead to cirrhosis and liver failure)

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65
Q

What are some intracellular accumulations due to injury?

A
  • Cholesterol
  • Protein
  • Pigments
  • Environmental particles
  • Fat
  • Water
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66
Q

What substance is the most damaging intracellular accumulation?

A

Cholesterol in the cells of arteries (atherosclerosis)

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67
Q

What is the most common pigment accumulation in damaged cells?

A

Lipofuscin “wear and tear” pigment

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68
Q

What happens to proteins in intracellular accumulation in injury?

A

Misfolded or otherwise abnormal proteins accumulate in a variety of diseases

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69
Q

What are some environmental particles that accumulate in injured cells?

A

Inhaled particles from cigarette smoke or polluted air

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70
Q

What is atrophy?

A

The decreased size and function of a cell, tissue, organ, or body part

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71
Q

What is atrophy a response to?

A

Decreased demand or to increased stress as the cell shuts down its metabolic processes to conserve energy

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72
Q

What is physiologic atrophy?

A

Normal part of life - thymus gland atrophies almost totally by puberty, muscles atrophy with age

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73
Q

What is pathologic atrophy?

A

Result of disuse or lack of normal physiologic support

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74
Q

What are some causes of atrophy?

A
  • Decreased size and function
  • Decreased functional demand
  • Inadequate nutrients
  • Aging
  • Interruption of trophic signals
  • Persistent cell injury
  • Increase pressure
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75
Q

What does atrophy of gastric mucosa result in?

A

Ulcer

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76
Q

What is a trophic signal?

A

A signal that stimulates the nourishment and growth of a tissue or cell

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77
Q

What is an example of a trophic signal?

A

estrogen keeps ligaments in the uterus and vagina taut

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78
Q

What is hyperplasia?

A

The enlargement of a tissue or organ owing to an increase in the number of cells

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79
Q

What can cause hyperplasia?

A
  • Hormonal stimulation
  • Chronic injury (calluses)
  • Increased functional demand
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80
Q

When does hypertrophy and hyperplasia occur together?

A

Enlargement of the uterus in pregnancy

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81
Q

What is an example of hyperplasia relating to estrogen?

A

Increased production of estrogen during puberty causes the endometrial lining to bulk for menstruation

82
Q

When does hyperplasia occur due to an increased functional demand?

A

Hyperplasia of the RBCs to compensate for decreased oxygen supply at a high altitude

83
Q

What is metaplasia?

A

Reversible change of one cell type into another caused by chronic injury

84
Q

Where is metaplasia most common in the body?

A

Epithelium

85
Q

What is the most common example of metaplasia?

A

Barrett esophagus - esophagus is usually squamous cell epithelium, but changes into gastric (columnar) epithelium due to chronic reflux of gastric acid

86
Q

Is Barrett esophagus reversible?

A

Yes - metaplasia is reversible, epithelium reverts to normal when the injury stops

87
Q

What is dysplasia?

A

“disordered growth” - refers to a premalignant change of cells

88
Q

What does dysplasia look like?

A
  • Variation in size and shape of cells, irregularity
  • Distorted cells
  • Large, dark nuclei (chromosomal chaos)
89
Q

What is dysplasia due to?

A

Disturbance to growth due to injury

90
Q

What is an example of dysplasia?

A

HPV causes dysplasia in the cervix (precancerous cervical cancer)

91
Q

When does dysplasia turn into cervical cancer?

A

Repeated HPV infections convert normal epithelium into increasingly severe dysplasia until malignant epithelium breaks through the basement membrane to become invasive cancer

92
Q

What is apoptosis?

A

Cells live out their natural life span and die by “natural suicide” in a carefully regulated, orderly process
Natural, physiologic, programmed cell death

93
Q

What is necrosis?

A

Pathologic death of cells due to injury or disease

94
Q

What signals a cell to undergo apoptosis, in terms of cellular structures?

A

Telomere on the end of a chromatid does not replicate, so each time the chromosome replicates, it loses a bit of the telomere. When the entire telomere is lost, it signals the cell that it is time to die

95
Q

What are the types of necrosis?

A
  • Coagulative
  • Liquefactive
  • Caseous
  • Fat
96
Q

What is coagulative necrosis?

A

Characterized by a gel like change in blocks of freshly dead cells - cells die in place without anatomic disruption, so tissue architecture is preserved despite death

97
Q

What is the most common type of coagulative necrosis?

A

Infarct

98
Q

What is liquefactive necrosis?

A

Cell death in which the dead tissue dissolves into fluid, because dead cells are disrupted or dissolved

99
Q

What is the most common type of liquefactive necrosis?

A

Abscess

100
Q

What happens with the development of an abscess?

A

Bacteria incites severe cell damage and attracts great numbers of WBC to secrete digestive enzymes, which in an effort to to kill the bacteria also digest dead cells into liquid pus

101
Q

What is caseous necrosis?

A

Variant form of coagulative necrosis with limited liquefaction and obliterated cellular detail

102
Q

What is the most common caseous necrosis?

A

Tuberculosis

103
Q

What is fat necrosis?

A

Specialized form of liquefactive necrosis that occurs only in fat

104
Q

Where is fat necrosis common?

A

Around the pancreas

105
Q

How does pancreatic disease involve fat necrosis?

A

Liberates pancreatic digestive enzymes that convert pancreatic fat into glycerol and fatty acids, which combine with calcium to form soap, trapping the calcium as tiny deposits in the injured tissue

106
Q

What is the goal of inflammation?

A

To return the tissue to normal, functioning tissue, limiting the extent of injury

107
Q

When is apoptosis especially important in early life?

A

Emryological development (webbed fingers)

108
Q

What mechanisms incite actual cell death during apoptosis?

A
  • External force stimulates suicide genes
  • External force inactivates other genes necessary to sustain cell life
  • Manufacture of suicide substances that attack cell
109
Q

How does a cell disappear after apoptosis?

A

The cell shrivels and is ingested and digested by macrophages

110
Q

What is acute inflammation the result of?

A

Comparatively severe, short term injury

111
Q

What is chronic inflammation the result of?

A

Comparatively mild, long term injury

112
Q

What is the initial inflammatory response?

A

VASCULAR!

113
Q

What is the name of the cells of inflammation?

A

Leukocytes

114
Q

What reaction follows the vascular response?

A

Cellular reaction

115
Q

What are neutrophils?

A
  • Multilobed nucleus
  • Main inflammatory cells in ACUTE inflammation
  • Main task is phagocytosis
  • Produce chemical messenger molecules
116
Q

What are eosinophils?

A

-Bilobed nucleus
-Principal inflammatory cells in parasitic infections
Attracted to allergic reactions

117
Q

What are basophils?

A
  • Attract other inflammatory cells during allergic reactions

- Contain histamine

118
Q

What is histamine?

A

Responsible for the local signs of allergic reactions (swelling, itching, vascular congestion, and mucus production)

119
Q

What is the tissue cell that is similar to a basophil?

A

Mast cell

120
Q

What are lymphocytes?

A
  • Single, large nucleus, scant cytoplasm
  • Made in bone marrow
  • Mature in lymphoid organs
  • B and T types
  • Main cells in CHRONIC inflammation
121
Q

What are plasma cells?

A

B lymphocytes that are actively making antibodies

122
Q

What are monocytes?

A
  • Large nucleus, large cell

- Made in bone marrow

123
Q

What cells do monocytes turn into?

A

After migrating into tissue, monocytes mature into macrophages

124
Q

What are platelets?

A

Fragments of cytoplasm of a bone marrow cel, the magekaryocyte

125
Q

What percentage of WBCs are neutrophils?

A

67%

126
Q

What percentage of WBCs are eosinophils?

A

0-3%

127
Q

What percentage of WBCs are basophils?

A

0-1%

128
Q

What percentage of WBCs are lymphocytes?

A

25%

129
Q

What percentage of WBCs are monocytes?

A

5%

130
Q

What are chemical mediators?

A

Injured cells release chemical signals that work together to produce inflammation, reduce the consequences of injury, and repair the damage

131
Q

What are autocrines?

A

Signals that act back on the generating cell

132
Q

What are paracrines?

A

Molecules released by cells that act on nearby cells

133
Q

What are endocrines?

A

(Hormones) Molecules released into the bloodstream to act on distant cells

134
Q

What do hormones (endocrines) released into inflamed tissues do?

A

Attract more inflammatory cells from nearby capillaries

  • Circulate blood to stimulate bone marrow to release addition leukocytes
  • Act on brain to increase body temperature (fever)
135
Q

What is the vascular response to inflammation?

A
  • Immediate, temporary contraction of local arterioles
  • Immediate dilation of arterioles, flooding capillaries with blood
  • Stretches spaces in seams between endothelial cells, allowing plasma to leak from blood into the tissues and neutrophils migrate through the gaps
  • Injured endothelial cells become sticky, and inflammatory cells stick to them
  • Plasma accumulates and the site swells
136
Q

Where does blood flow fastest in the vessel?

A

In the center

Slower at sides due to friction of the wall

137
Q

How do leukocytes stay at the site of injury?

A

Slow moving leukocytes along the capillary wall begin to stick to the lining endothelial cells (injured endothelial cells become sticky)

138
Q

What happens to blood flow when arterioles dilate after injury?

A

Increased blood flow due to dilation, but flow slows because vessel is so enlarged (WBCs settle out or sludge along the edges)

139
Q

What comprises the inflammatory exudate?

A

Accumulated edema and inflammatory cells at the injured site

140
Q

What are the characteristics of acute inflammation?

A

Tumor - swelling
Rubor - redness
Calor - heat
Dolor - pain

141
Q

Why does redness appear?

A

Increased blood flow

142
Q

Why does edema appear?

A

Increased fluid from leaky vessels

143
Q

What substance do platelets release?

A

Serotonin

144
Q

What substance do mast cells release?

A

Histamine

145
Q

What substance do injured cells release?

A

Prostaglandins

146
Q

What substance slows blood flow?

A

Bradykinin

147
Q

What cells are associated with acute inflammation?

A

Neutrophils

148
Q

What cells are associated with chronic inflammation?

A

Lymphocytes

149
Q

What do histamine and serotonin do to vessels?

A

Increase capillary permeability

150
Q

What is serous inflammation exudate?

A

Copious amounts of watery fluid that is low in protein and has few inflammatory cells; seen in mild, short term inflammation

151
Q

What is an example of serous inflammation?

A

Blister, oozing fluid from superficial skin burn

152
Q

What is fibrinous inflammation exudate?

A

Characterized by thicker, wetter exudate containing more neutrophils and coagulation factors that form a web of fibrin; seen with more severe injury

153
Q

What is an example of fibrinous inflammation?

A

Scav of superficial skin injury

154
Q

What is purulent/pyogenic/suppurative inflammation exudate?

A

Characterized by creamy fluid (pus) composed of necrotic debris and many neutrophils; seen with severe cute injury;

155
Q

What is an example of suppurative inflammation?

A

Abscess

156
Q

What type of necrosis is purulent inflammation associated with?

A

Liquefactive

157
Q

What are the outcomes of an acute inflammation?

A
  • Complete resolution
  • Scarring
  • Abscess
  • Chronic inflammation
158
Q

What are some causes of chronic inflammation?

A
  • Persistent infection
  • Autoimmune disease
  • Persistent exposure to injurious agents
159
Q

Does chronic inflammation show the four typical characteristics of acute inflammation?

A

Chronic inflammation is less intense, and therefore is usually not as hot, swollen, red, or tender

160
Q

What is granulomatous inflammation?

A

Special type of chronic inflammation where sheets of macrophages aggregate around a central group of necrotic cells or an infectious microorganism to form tiny inflammatory nodules called granulomas

161
Q

Why does chronic inflammation involve a rich blood supply?

A

Because chronic inflammation is the mixture of ongoing inflammation and healing

162
Q

What are some examples of causes of granulomatous inflammation?

A
  • Smoking
  • Tuberculosis
  • Specific autoimmune diseases
163
Q

What are three distant effects of inflammation?

A
  • Systemic effects like fever, myalgia
  • Involvement of lymphatics
  • Production of reactant proteins
164
Q

What is lymphadenopathy?

A

Enlarged or tender lymph nodes

165
Q

What is reactive hyperplasia of lymph nodes?

A

Enlarged or tender lymph nodes, often due to a reaction to inflammatory products draining away from an infection or injury

166
Q

What is CRP?

A

C-reactive protein, a reliable marker for current inflammation

167
Q

Where is CRP made?

A

Liver

168
Q

What is fibrinogen?

A

Coagulation protein that polymerizes into the meshwork of fibrin in a blood clot

169
Q

What is ESR?

A

Erythrocyte sedimentation rate - increased fibrinogen causes RBCs to settle rapidly in their own plasma

170
Q

How does fibrinogen relate to inflammatory response?

A

Inflammatory mediators stimulate the liver to manufacture fibrinogen

171
Q

What is the extent of ESR increase proportional to?

A

The degree of inflammation in the patient

172
Q

What is repair?

A

The body’s collective attempt to restore normal structure and function to the injured site

173
Q

What is a wound?

A

An injury result in from short term injury at a discrete site

174
Q

What is stroma?

A

Supporting tissue

175
Q

What two processes make up the process of repair?

A

Regeneration and healing

176
Q

What is regeneration?

A

The complete restoration of normal anatomy and function by the regrowth of normal functional cells and supporting tissue

177
Q

What is parenchyma?

A

Normal functioning cells

178
Q

What is healing?

A

A mix of regeneration and scarring, or scarring alone if regeneration is not possible

179
Q

Why are macrophages important in repair?

A

They linger the longest at the site and act to stimulate growth of connective tissue cells

180
Q

Do parenchymal cells participate in fibrous repair?

A

No - parenchymal cells are involved in cellular regeneration

Fibrous repair is used if regeneration is not possible

181
Q

What is the first stage in fibrous repair?

A

Cell migration - proliferation of myofibroblasts to make collagen

182
Q

What is the second stage in fibrous repair?

A

Angiogenesis

183
Q

What is the third stage in fibrous repair?

A

Scar development - synthesis of collagen fibers to knit together disrupted tissue

184
Q

What substance stimulates angiogenesis?

A

Vascular endothelial growth factor

185
Q

What is granulation tissue?

A

Collagen and the new capillaries that form in fibrous repair (the fragile pink tissue under a scar, prone to bleeding)

186
Q

What is first intention?

A

The healing of narrow wounds with closely approximated edges

187
Q

What is second intention?

A

Healing of broad wounds with widely separated margins

188
Q

Do first and second intention heal by different mechanisms?

A

No, follow same steps of repair

189
Q

How do the margins of wounds pull together to heal?

A

Myofibroblasts generate a matrix of collagen and other fibers to bind together the edges of the wound, then contract, pulling the edges of the wound inward

190
Q

What happens to the blood vessels formed by angiogenesis during fibrous repair?

A

Eventually they shrink or disappear as the workload decreases

191
Q

What does a scar look like after complete remodeling?

A

Mechanical forces pull the scar into a configuration that eases stress on the wound, so it fits comfortable in the site, in conformity to surrounding tissue

192
Q

How does angiogenesis occur?

A
  • Basement membrane of injured capillaries dissolves
  • Endothelial cells migrate through defect and into injury
  • Proliferate to form a new capillary
193
Q

What factors interfere with wound healing?

A
  • Infection
  • Poor nutrition
  • Steroid drugs
  • Diabetes
  • Poor vascular supply
  • Foreign objects
  • Mechanical forces
194
Q

How does poor nutrition effect wound healing?

A

Deficiency of vitamin C or proteins inhibits collagen synthesis

195
Q

How do steroids effect wound healing?

A

They slow the growth of myofibroblasts and the production of collagen

196
Q

What does dehiscence mean?

A

If a wound does not heal properly, it may rupture

197
Q

What are two types of pathologic wound hewing?

A

Keloid and pyogenic granuloma

198
Q

What is a keloid?

A

Hyperplastic scar that is prominent, raised, or nodular, and that contains excess collagen

199
Q

What is a pyogenic granuloma?

A

Localized, highly vascular collection of persistent granulation tissue, often losing inflammatory infiltrate and edema fluid, giving them exceptional vascularity

200
Q

Why does diabetes effect wound healing?

A

Diabetes influences the vascular system, with constant inflammation in arteries, causing impaired blood flow

201
Q

What kind of mechanical forces often interfere with healing of a wound?

A

Coughing, sneezing, laughing

From Flashcardlet (133 decks)

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