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7 PATH 1 > Cellular Component > Flashcards

Cellular Component Flashcards

1
Q

What are the 5 types of blood cells?

A 
Neutrophils
Eosinophils
Basophils
Lymphocytes
Monocytes
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2
Q

What are Polymorphonuclear cells aka

A

Granulocytes

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3
Q

What are the Polymorphonuclear aka granulocytes?

A

Neutrophils, Eosinophils, and Basophils

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4
Q

What does it mean to be Polymorphonuclear aka granulocyte?

A

All have granules visible under light microscope and have several lobes in their nucleus

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5
Q

What is the % of Nucleus?

A

55-60% (most common)

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6
Q

What is characteristic of Neutrophils?

A

1st to arrive at site of inflammation (1st line of defense)

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7
Q

Are neutrophils phagocytic?

A

YES

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8
Q

What is the lifespan of neutrophils?

A

8hr - 3 days

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9
Q

What are characteristic of Eosinophils?

A

Red granules in cytoplasms with pink color and have 2 lobes of nuclei

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10
Q

What is Eosinophil %?

A

2-4%

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11
Q

Are eosinophils phagocytic?

A

YES

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12
Q

Basophils have what characteristic?

A

Blue Granules with 2 lobes

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13
Q

Basophil %?

A

.5 - 1 %

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14
Q

Are basophils phagocytic?

A

NO

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15
Q

What is special quality of basophils?

A

They release histamine (with mast cells)

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16
Q

Mononuclear aka

A

Agranulocytes (no granules seen under light microscope)

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17
Q

What are the 2 Mononuclear aka agranulocytes?

A

Lymphocytes and Monocytes

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18
Q

Lymphocytes % ?

A

20-25%

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19
Q

Lymphocytes are _____

A

antibodies

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20
Q

Monocytes % ?

A

4-8 %

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21
Q

What is characteristic of Monocytes?

A

Largest cells in blood

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22
Q

What is the life span of monocytes?

A

YEARS

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23
Q

What is the process of action in inflammation?

A

Neutrophils and monocytes are the 2 cells that go into the site of inflammation.

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24
Q

What do neutrophils do during Inflammation?

A

They are the most abundant (high peak in curve) but their lifespan is short

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25
Q

What do monocytes do during inflammation?

A

Monocytes come in after neutrophils and when they do they receive the name (macrophage) APC and their function is to phagocytose bacteria

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26
Q

What are the stages of Phagocytosis?

A

1) Recognition
2) Engulfing
3) Indigestion
4) Exocytosis
5) Exposure of a fragment on the surface of the phagocytic cell (MHC II)

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27
Q

What is Recognition?

A

Recognition of bacteria and attachment to the site done by Chemotaxis

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28
Q

What is Engulfing?

A

With use of pseudo pods and formation of vesicles

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29
Q

What is indigestion?

A

Killing and degredation/fragmentation by lysosomal enzymes

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30
Q

What is exocytosis?

A

Removal of the fragments

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31
Q

What is the 5th step in phagocytosis?

A

Exposure of a fragment on the surface of the phagocytic cell (MHC II)

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32
Q

What are the Phagocytic cells?

A

MEN

neutrophils, monocyte/macrophage, and basophils

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33
Q

What are the 2 types of Phagocytosis?

A

Oxygen independent and dependent

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34
Q

What happens during Oxygen independent phagocytosis?

A

Lysosomes in macrophages produce and secrete protein that are able to kill intruder

Lysozyme: digests chemical bond of cell wall

Elastase: Digests elastic fibers

Collagenase: Digest collagen

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35
Q

What are the 2 enzymes of Oxygen independent phagocytosis?

A

Enzymes of Macrophages and Neutrophils

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36
Q

What are enzymes of Neutrophils?

A

Defensin - antibody like substance produced in the lysosomes of neutrophils (primary line of defense) (kills the bacteria)

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37
Q

What is Oxygen dependent Phagocytosis mean?

A

Production of free radicals

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38
Q

What is the production of free radicals?

A

Found in granules of phagocytic cells and it has its effect on the lipid mb of the foreign cell

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39
Q

What are the 3 things associated with Production of free radicals? (oxygen dependent phagocytosis)

A
  • Superoxide anion
  • Hypochlorite anion
  • Hydrogen Peroxide (H2O2)
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40
Q

How is Hydrogen Peroxide Effective?

A

It kills bacteria by releasing oxygen but this causes the release of alcohol. Mechanical removal due to bubbling and painless process

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41
Q

What are the 2 defects associated with Leukocyte Function?

A

1) Chronic Granulomatous disease of children

2) Chediak-Higashi Syndrome

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42
Q

What is Chronic Granulomatous Disease of children?

A

Rare genetic disorder.

The child’s phagocytic cells (all of them) are not able to produce free radicals (no oxygen dependent phagocytosis)

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43
Q

What happens in Chronic Granulomatous Disease of children?

A

Child dies at 2 years old due to infection because the mechanism of killing parasites is not present

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44
Q

What is Chediak-Higashi Syndrome?

A

Genetic Disease.

Impairment of phagocytic cell motility = cannot go to the site of infection at proper time

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45
Q

What is the major problem with Chediak Higashi Syndrome?

A

WBC’s are not able to degranulate (release lysozyme from granules)

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46
Q

What happens to children in Chediak Higashi syndrome?

A

They die at 1.5 - 2 due to infection

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47
Q

What does inflammation need?

A

Initiatior and mediator cells

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48
Q

What are the 7 initiators of Inflammation?

A

1) Direct stimulus to mast cells
2) Microbial Products
3) Exposure of basement membrane or connective tissue components
4) Complement activation
5) Deposition of antibody/antigen complexes
6) Disruption of vascular integrity
7) Substances released from injured cells

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49
Q

What are the Types of cell mediators: Cell derived and plasma derived? **

A

1) Mediators cell-derived of inflammation

2) Mediators of inflammation plasma derived

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50
Q

What are the Cell Derived Mediators of Inflammation ?

A
  • Histamine
  • Seratonin
  • Substance P
  • Nitric Oxide/Endothelial-Derived Relaxing Factor
  • Eicosanoids
  • Tumor Necrosis Factor (TNF)
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51
Q

Where is Histamine released?

A

Near the site of inflammation

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52
Q

Where is Histamine released from?

A

Granules of mast cells, basophils or platelets in response to physical injury (trauma, heat, cold) or type 1 Hypersensitivy reaction (allergy)

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53
Q

When would Histamine be released?

A

In response to physical injury or Type 1 hypersensitivity reaction (allergy)

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54
Q

Histamine is released in a process of ______

A

Degranulation

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55
Q

Where is Histamine released from?

A

Basophils into blood circulation, mast cells are basophils that are fixed in tissues and platelets. Major reservoir of histamine in the body

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56
Q

What are the 4 functions of Histamine?

A

1) Vasodilation
2) Increase permeability of vessels (endothelial retraction)
3) Bronchospasm
4) Increase Mucous Production

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57
Q

What is vasodilation?

A

Relaxation of smooth muscle cells in their sphincters of arterioles (increasing blood flow to capillary bed)

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58
Q

What is bronchospasm?

A

Narrowing of bronchial lumen of respiratory tree

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59
Q

How do you increase mucous production?

A

Increase by the mucous gland in trachio bronchial tree

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60
Q

What are the causes of mast cell degranulation?

A

Physical injury, high/low Ta or Type 1 allergic Reactions –> anaphylotoxins C3a and C5a cause degranulation, neuropeptides (substance P) and cytokines

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61
Q

Serotonin aka

A

Hormone of pleasure

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62
Q

Serotonin is produced by _____

A

platelets

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63
Q

Serotonin functions are similar to _____

A

Histamine

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64
Q

What is Substance P (neuro peptide) produced by?

A

Nervous fibers, peripheral and Central NS (Protection)

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65
Q

What area of the body is substance P- neuro Peptide produced by?

A

Lungs and Gastrointestinal Nervous tissues

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66
Q

What is the function of Substance P - neuropeptide?

A

1) Promotion of nerve conduction for production of pain
2) Regulate BP
3) Increase permeability of blood vessels

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67
Q

Nitric Oxide aka

A

Endothelial derived relaxing factor (EDRF)

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68
Q

What is Nitric oxide aka Endothelial Derived Relaxing Factor (EDRF) produced by?

A

Endothelial cells of blood vessels (inner surface of blood vessels), macrophages, and brain neurons

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69
Q

What does Nitric Oxide aka EDRF cause?

A

Smooth Muscles to relax

70
Q

What is Nitric Oxide a mediator of?

A

Sympathetic Nervous system ( ~ 10%)

71
Q

What are the functions of Nitric Oxide?

A

1) Vasodilation
2) INHIBITION of the recruitment of neutrophil to the site of inflammation
3) Inhibits the cellular component of inflammation: Inhibit adhesion of WBC’s to endothelial cells (PAVEMENTING)

72
Q

What are Eicosanoids?

A

They are Arachadonic acid metabolites

73
Q

Where do Eicosanoids come from?

A

Phospholipids of cell membranes

74
Q

What are Eicosanoids made from?

A

Neutrophils and Macrophages

75
Q

What is under the category of Eicosanoids?

A
  • Prostaglandins
  • Leukotrienes
  • Lipoxins
76
Q

What is under the category of Prostaglandins?

A
  • PGD2
  • PGE2
  • PGF2
  • Prostacyclin (PGI2)
  • Thromboxane A2 (TXA2)
  • All PGs made by 2 enzymes:
    1) COX 1
    2) COX 2
77
Q

What is the common denominator in PGD2, PGE2, and PGF2?

A

They all vasodilator and potentiate edema

78
Q

Where is PGD2 produced?

A

In Mast cells

79
Q

What does PGD2 induce?

A

Bronchospasm (asthma)

80
Q

What does PGD2 inhibit?

A

Hair growth (alopecia and baldness in men)

81
Q

What are the roles of PGE2?

A
  • Promotes Hyperalgesia (pain)
  • Induces fever
  • Induces LABOR by stimulating uterine contraction and relaxing the cervix
82
Q

What 2 PGE’s induce labor?

A

PGE2 and PGF2

83
Q

What does PGF2 do?

A

Causes the Corpus Luteum to undergo Luteolysis, this stops progesterone production, and induces labor (miscarriage)

84
Q

What is Prostacyclin aka

A

PGI2

85
Q

What is Prostacyclin aka PGI2 produced by?

A

Endothelial cells

86
Q

What does Prostacyclin aka PGI2 do?

A

Inhibit platelet aggregation and causes vasodilation

87
Q

Thromboxane A2 aka

A

TXA2

88
Q

What is Thromboxane A2 (TXA2) produced by?

A

Platelets

89
Q

What is the function of Thromboxane A2 (TXA2)?

A

Antagonist of PGI2

90
Q

What does Thromboxane A2 (TXA2) do?

A

Causes vasoconstriction (prevents blood loss) and PROMOTES platelet aggregation

91
Q

All Prostaglandins are _____

A

Produced via 2 enzymes called cyclooxyrgenases in response of inflammation

92
Q

What does COX-1 do?

A

Produces normal amounts of PG’s, and regulates amount of fluid and salt in kidneys

93
Q

What does COX1 protect?

A

GI tract from ulceration and irritation

94
Q

Inhibitors of COX 1 ______

A

ALSO inhibit COX2

95
Q

What are examples of COX1 inhibitors?

A

NSAIDS, EX:

  • ibuprofen (advil)
  • Naproxen (aleve)
  • Indomethacin and aspirin
96
Q

What can COX1 inhibitors lead to?

A

Kidney problems and stomach irritation/ulceration due to overproduction of HCL

97
Q

What does Inhibitors of COX1 cause?

A

Swelling due to impairment of water and salt regulation

98
Q

What does COX-2 Produce?

A

Extra prostaglandins when needed in addition to the already existing from COX1

99
Q

What are examples of COX2 inhibitors?

A

Vioxx, celebrex, meloxicam

100
Q

What are COX-2 inhibitors side effects?

A

Vioxx could result in thrombosis, thromboaneurysm, MI

101
Q

For normal amount of inflammation ______

A

Body produces enough prostaglandins via COX-1, when more than normal is needed, extras are produced via COX-2

102
Q

What are Leukotrienes qualities?

A
  • Vasoconstriction and balance out vasodilator
  • Bronchospasm
  • Increased Permeability
103
Q

What is the enzyme that creates Leukotrienes?

A

5 - Lipoxygenase

104
Q

What do Lipoxins do?

A
  • Vasodilation
  • Inhibits Neutrophil chemotaxis
  • Stimulates monocyte adhesion
105
Q

What is the enzyme that creates Lipoxins?

A

12 - Lipoxygenase

106
Q

What are Eicosanoid inhibited by?

A

Steroids

107
Q

What do steroids inhibit?

A

The production of arachidonic acid = No Prostaglandins, Leukotrienes, or Lipoxins

(By INHIBITION of Phospholipase)

108
Q

What are the most potent inflammatory suppressor?

A

Corticosteroids

109
Q

What is tumor necrosis factor Produced by?

A

Activated macrophages and T helper cells

110
Q

What does tumor necrosis factor interfere with?

A

The immune response accounting with the prevention of tumors

111
Q

What does Tumor Necrosis Factor induce?

A

Acute inflammatory response

112
Q

What is Tumor Necrosis factor Medication for?

A

RA, ankylosing Spondylitis, etc.

  • Inhibit TNF and my lead to LYMPHOMAS
113
Q

Inhibitng TNF can lead to _____

A

Production of malignant tumors, and it suppresses the immune system

Increases susceptibility to TB and Herpes Zoster

114
Q

Each cascade stimulated by the activation of _____

A

Haegman Factor (clotting factor 12)

115
Q

What are the categories under “Plasma Derived Mediators?”

A

1) Complement system
2) Kinin System
3) Coagulation system/clotting cascade
4) Fibrinolysis system

116
Q

What does the complement system create?

A

A cascade of chemical reactions that promotes opsonization, chemotaxis, and agglutination, and produces the MAC

117
Q

What do antibodies do in regard to the complement system?

A

They are NOT part of the cascade reaction, but they PROMOTE INFLAMMATION. They come from plasma in nature

118
Q

What do Anaphylotoxins C3a, C4a, and C5a refer to?

A

The fragment that has been separated from the complement part

119
Q

What do Anaphylotoxins C3a, C4a, and C5a promote?

A

Degranulation of mast cells and basophils and the secretion of histamine from granules

120
Q

What does C5a promote?

A

The production of 5-lipoxygenase activating the pathway of leukotrienes

121
Q

What does the Kinin System do ?

A

Generates protein capable of sustaining vasodilation and other physical inflammatory effects –> BRADYKININ

122
Q

What does the Coagulation System of Clotting Cascade do?

A

Forms a protective protein mesh over sites of injury –> THROMBIN

123
Q

What does the Fibrinolysis System do?

A

Acts in opposition to the coagulation system, to counterbalance clotting and generate several other inflammatory mediators –> PLASMIN.

124
Q

What does the Fibrinolysis system activate?

A

FXII (negative Feedback)

125
Q

What is the Hageman Factor (Clotting Factor XII)?

A

A protein that circulates inactively

126
Q

What activates Hageman Factor (Clotting factor XII)?

A

Collagen, platelets, or exposed basement membranes via conformational change

127
Q

What is the Hageman factor able to do when it is activated?

A

Able to activate 3 plasma systems involved in inflammation: The kinin system, fibrinolysis system, and coagulation system.

128
Q

What does Bradykinin cause?

A

Vasodilation, promotes the vascular component of the inflammation, increased permeability of the vessel via Prostacyclin and NO.

129
Q

What is Bradykinin?

A

A small peptide with short life, very unstable that is destructed 5 min after creation (after 5-10 min)

130
Q

When does lymph become the name, “Lymph?”

A

Same interstitial fluid but within the capillary vessels

131
Q

What happens during acute inflammation in the lymphatic system?

A

Lymph also has valves and when the compartments are full with fluid, the pressure opens the valves and fluid moves distal to proximal, and fluid ends in lymph nodes where immune cells reside (triggering an immune response)

132
Q

What is Lymphangitis?

A

Inflammation of a lymphatic vessel, it appears as a red line

133
Q

During Lymphangitis, what happens?

A

Infection goes to interstitial fluid –> lymphatic capillaries-> inflammation of lymphatic vessels

134
Q

What does Lymphangitis cause?

A

Enlarged and painful nodes (if not painful, then metastatic cancer)

135
Q

If the immune system is supressed, what can lymphangitis develop into?

A

Lymphadenitis

136
Q

What is Lymphadenitis?

A

Enlarged and painful (inflamed) lymph nodes from accumulation of bacteria

137
Q

Where can Lymphadenitis spread?

A

Into the rest of lymphatic nodes - systemic circulation - end up in the vena cava

138
Q

What is Bacteremia?

A

Bacteria in blood

139
Q

What can bacteremia cause?

A

Septicemia

140
Q

What is Septicemia?

A

Accumulation of toxic products from bacteria metabolism in blood

141
Q

What does Bacteremia cause?

A

Leukocytosis (Increase in WBC’s more than 9000 leukocytes)

142
Q

Neutrophil %

A

55-60

143
Q

Lymphocyte %

A

20-25

144
Q

Monocyte %

A

4-8

145
Q

Eosinophil %

A

2-4%

146
Q

Basophil %

A

.5 - 1

147
Q

What is Leukocytosis?

A

Increase leukocytes in blood ( > 9000 per 1 cubic mm) due to infected blood

148
Q

What is Netrophilia?

A

More than 60% indicates acute Bacterial Infection (acute appendicitis)

149
Q

What would Lymphocytosis indicate?

A

Possible Viral Infection

150
Q

What would Eosinophil indicate?

A

Allergic Reactions (Type I Hypersensitivty reactions) and Parasitic Infections (WORMS)

151
Q

What would Monocytosis indicate?

A

Chronic bacterial infection (can increase up to 50% of circulating WBCs)

152
Q

What can Monocytosis be?

A

Infectious mononucleosis and Lymphadenopathy of neck and upper thoracic lymph nodes

153
Q

Is there Exudate in chronic inflammation?

A

NO, (exudate is only in acute)

154
Q

What is the cell content of chronic inflammation?

A

Only consists of cell that live long: Monocytes/Macrophages and lymphocytes

155
Q

What are 5 agents typically involved in chronic inflammation?

A
  1. Mycobacterium TB
  2. Mycobacterium Leprae - leprosy
  3. Listeria Species - Listeriosis
  4. Treponema Pallidum - Syphilis
  5. Brucella Species - Brucellosis
156
Q

What does Chronic inflammation arise due to?

A
  • Viral infection
  • persistent microbial infection
  • Prolonged exposure to potentially toxic substances
  • Autoimmune diseases
157
Q

What is Non specific chronic inflammation?

A

A diffuse accumulation of macrophages and lymphocytes develops at site of injury

158
Q

What is an example of Non specific chronic inflammation?

A

Inorganic material (silica) cannot be digested causing Silicosis.

159
Q

If silica or silicosis goes into the lungs what can happen?

A

They can go into the lungs where the enzymes will try to digest it causing Pneumoconiosis

160
Q

What is Pneumoconiosis?

A

Silicosis and Asbestosis

161
Q

What is Pneumoconiosis?

A

Lung disease from inhalation of industrial toxic, fume

162
Q

What happens during Pneumoconiosis ?

A

Tissue is damaged and replaced with scar tissue

163
Q

What are the 2 types of Chronic inflammation?

A

1) Nonspecific Chronic inflammation

2) Granulomatous Inflammation

164
Q

What is nonspecific chronic inflammation?

A

A diffuse accumulation of macrophages and lymphocytes develops at the site of injury

165
Q

What are 2 examples of non specific chronic inflammation?

A

Pneumoconiosis and Silicosis

166
Q

What is granulomatous Inflammation?

A

Development of granulomas that contain the bad boys

167
Q

What are epithelial cells?

A

Activated macrophages

168
Q

What are multinucleate giant cells?

A

Many macrophages joined together

169
Q

What does IFN-8 do for granulomatous inflammation?

A

Promoted the production of both epithelioid cells and multinucleate giant cells

170
Q

Where is a typical example of Granulomatous Inflammation seen?

A

In primary TB complex

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