Exam 2 Flashcards

1
Q

What is inflammation

A

An adaptive response to injury or illness that brings fluid (plasma), dissolved substances, and blood cells into the interstitial tissues where the invasion or damage has occurred.

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2
Q

What type of response is inflammation and what does it mean?

A

Is a nonspecific response - same events occur regardless of cause of inflammatory process.

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3
Q

What are the microorganisms that cause inflammation?

A
  • bacteria
  • viruses
  • fungi
  • helminths
  • protozoans
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4
Q

What chemical agents can cause inflammation (2)

A

HCL (internal) or poisons (external)

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5
Q

What physical agents can cause inflammation (2)

A

Objects that cause trauma to skin, excessive heat or cold and radiation

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6
Q

What is the ACUTE inflammatory process?

A
  • Response occurs within minutes of injury or with infection may be a few hours
  • Erythema, heat swelling, pain and impaired function occur
  • Continues until trauma or infection is neutralized
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7
Q

What is the CHRONIC inflammatory process?

A
  • Occurs when the acute response is unable to neutralize the harmful stimuli
  • Causes damage to healthy tissue – scarring
  • Seasonal allergic reactions or autoimmune disease
  • Can follow acute but usually does not.
  • Diseases of chronic are COPD and SLE
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8
Q

1st Stage: Vascular and Cellular response
- What happens to blood vessels?
- What do injured tissue release?
- What is hyperemia and what is it responsible for?
- Does vascular permeability increase or decrease?

A
  • Blood vessels temporarily constrict the surrounding area
  • Injured tissue releases histamines, kinins, and prostaglandins
  • Chemical mediators to dilate blood vessels
  • Causes an increase in blood flow to injury
  • Hyperemia - a marked increase in blood supply
  • Responsible for erythema (redness) and heat noted in inflammation
  • Vascular permeability increases
  • Dilated vessels cause blood flow to slow
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9
Q

What happens when vascular permeability increases?
What does this cause?

A
  • fluids, proteins, and leukocytes (WBCs) leak into interstitial spaces
  • causes swelling and pain
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9
Q

What happens when Dilated vessels cause blood flow to slow

A
  • Allows more leukocytes to injured area
  • Margination occurs - Leukocytes roll along vessels walls, detach and bind again
  • Leukocytosis - Drop in circulating leukocytes stimulates bone marrow to produce and release more into blood stream
  • WBC counts can reach 20,000/mm3 (Normal WBC 4,500 to 10,000 per mm3)
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10
Q

What is the 2nd stage of inflammation?

A

Exudate Production

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11
Q

In the exudate production (2nd stage), what is contained in the fluid that leaks

A

cytokines, histamines, dead tissue cells, injured tissue cells, and dead phagocytic cells
- Amount is dependent on tissue involved, amount of damage and length and intensity of the initial inflammatory process

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12
Q

for 2nd stage, what types of exudate is there? (3)

A
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13
Q

What is the name of the 3rd stage of inflammation?

A

Reparative Phase

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14
Q

What happens in the 3rd stage of inflammation?

A
  • Chemical mediators to assist damaged cells in repairing themselves
  • Regeneration occurs - Destroyed cells are replaced with cells identical or similar in structure and are replaced one by one so that the architectural pattern and function of the tissue is restored
  • Some tissues regenerate quickly - epithelial tissues of skin, digestive system, respiratory system
    Some tissues have limited capacity to regenerate – nervous, muscular and elastic tissues
  • Scar tissue – fibrous tissue formation occurs when regeneration is not possible
    -Early process is granulation tissue
    -Does not function as original tissue – can lead to complications
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15
Q

What are macrophages?

A

secrete factors that remove pathogens by phagocytosis- Secrete Cytokines that attract immune system cells

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16
Q

What are Mast Cells

A
  • Leukocytes found in most tissues of the body
  • Principle source of cell-derived mediators of inflammation
  • Secrete factors that mediate dilation and constriction of blood vessels
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17
Q

What are the (6) chemical mediators?

A
  • Histamine
  • Heparin
  • Leukotrienes
  • Prostoglandins
  • Bradykinin
  • Complement
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18
Q

What is a Histamine?

A

A chemical mediator stored and released by mast cells
- Contributes to early vasodilation, increased permeability and chemically attracts eosinophils (4 types of receptors)

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19
Q

What is Heparin

A
  • Also released and with histamine increase blood flow to the injured site - dec. blood clotting to injury
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20
Q

What are Leukotrienes

A

Chemically attracts neutrophils and macrophages. Stored and released by mast cells

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21
Q

What are Prostaglandins

A

Present in most tissue
- Causes vasodilation
- stored and released by mast cells

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22
Q

What are Bradykinin?

A

Causes dilation of vessels, acts with prostaglandins to cause pain, increase vascular permeability and stimulates histamine release

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23
Q

What is a Compliment (for mediators of inflammation)

A

Comprises over 20 proteins, activated sequentially and is responsible for dilation, permeability, chemotaxis, phagocytosis and histamine release

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24
Q

What are the 4 types of Histamine receptors?

A

H1, H2, H3, H4

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25
Q

H1 receptor found primarily on what?

A

smooth muscle cells, endothelium, and CNS
Stimulation- vasodilation

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26
Q

H4 is located in what?

A

Peripheral WBCs and mast cells
- involved in immune response

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27
Q

Antihistamine block histamine = ?

A

decrease allergy symptoms

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28
Q

What occurs when an individual is exposed to the allergen that results in the rapid release of inflammatory mediators

A

Anaphylaxis

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29
Q

What is an autoimmune disorder?

A

the body misinterpreting its own tissue as harmful

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30
Q

what involves genes that regulate cytokines pathways

A

Genetic Consideration and nonmodifiable risk factors

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31
Q

What is the normal ESR levels

A

0-15 mm/hr, 0-20 mm/hr (women)

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32
Q

What is the cause of leukocytosis

A

infection, inflammation, leukemia, trauma or stress

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33
Q

What is immunity?

A

Body’s natural or induced response to infection

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34
Q

3 functions of the immune system

A
  • protect body from foreign antigens
  • identify; and destroy potentially harmful cells
  • Remove cellular debris
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35
Q

what is immunocompetent

A
  • an effective immune system
  • able to identify antigen and effectively destroy or remove them
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36
Q

what is hypersensitivity immunity?

A

overreaction of the immune system

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37
Q

What is an autoimmune disorder

A
  • immune system attacks own body
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38
Q

what is immunodeficiency

A
  • incompetent immune system
  • acquired immunodeficiency syndrome (AIDS)
  • system deficit induced by infection with HIV
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39
Q

What is an opportunistic infection?

A
  • infections that would not affect people with intact immune system
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40
Q

How does active immunity work?

A

it occurs through:
- exposure to disease
- vaccination
- long-lasting, often lifelong
- takes several weeks to develop

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41
Q

How does passive immunity work?

A

it occurs through:
- Receiving antibodies from another person
- ex: mother to newborn
- provides immediate protection
- lasts only weeks/months

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42
Q

Leukocytes overview description

A
  • WBC
  • the primary cells in both nonspecific and specific immune responses
  • derived from stem cells in bone marrow
  • attacks, and destroys anything “foreign” (damaged tissue and infection)
    –> Respond to released chemicals from other leukocytes and damaged tissue
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43
Q

Can leukocytes move through tissue spaces?

A

yes

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44
Q

What are the normal levels of leukocytes?

A

4500-10,000 cells/mm3

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45
Q

what cell adheres to vascular epithelial cells in vessel walls, and other tissue spaces within the lymphatic system

A

leukocytes

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46
Q

what level of leukocytes is leukocytosis

A

more than 10,000/mm3

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47
Q

what is leukocytosis

A

when there is a release of WBCs by bone marrow to respond to a threat

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48
Q

what is leukopenia

A

a decrease in the number of circulating leukocytes
- when bone marrow activity is suppressed
- when leukocyte destruction increases

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49
Q

What are the 3 major groups of leukocytes?

A
  1. Granulocytes
  2. Monocytes
  3. Lymphocytes
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50
Q

Where are granulocytes derived from?

A
  • from myeloid stem cells in bone marrow
  • instrumental in inflammatory response
  • 3 types: neutrophil, eosinophil and basophil
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51
Q

Where are monocytes derived from?

A
  • from myeloid stem cells in bone marrow instrumental in bone marrow
  • inflammatory response
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52
Q

Where are lymphocytes derived from?

A

derived from lymphoid stem cells in bone marrow
- Primary cells involved in the specific immune response

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53
Q

what is the name of the largest leukocytes?

A

monocytes

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54
Q

what consists of 60-80% of leukocytes

A

granulocytes

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55
Q

which leukocyte has a short lifespan

A

granulocytes

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56
Q

what is 2-3% of circulating leukocytes?

A

monocytes

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57
Q

what leukocyte states for months/years until it is activated

A

monocytes

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58
Q

what leukocyte is a memory cell

A

lymphocytes

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59
Q

Which Granulocyte is the most plentiful and consists of 55-75% of granulocytes?

A

Neutrophil

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60
Q

Neutrophil desc.

A

Phagocytic: Engulf, destroy foreign agents
—> first arrive at site of invasion

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61
Q

Which granulocyte is involved in hypersensitivity response —> inactivate some inflammatory chemicals released during inflammatory process

A

Eosinophils
- less efficient than neutrophils as phagocytes

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62
Q

What granulocyte is found in large #’s in the respiratory and GI tracts

A

Eosinophils

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63
Q

Which granulocyte is not phagocytic?

A

Basophils

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64
Q

Which granulocyte contains proteins and chemicals like heparin, histamine, bradykinserotonin, and leukotrienes

A

Basophils

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65
Q

Which granulocyte has an acute hypersensitivity or stress response?

A

Basophils

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66
Q

What type of monocytes differ by which tissue they reside?

A

Macrophages

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67
Q

Which monocyte activates the immune response against chronic infections

A

Macrophages

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68
Q

Which monocyte originates in the myeloid, lymphoid cell lines
- antigen-presenting cells
- operate in most organs?

A

Dendritic cells

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69
Q

What are Langerhans cells?

A

Specialized dendritic cells in the skin

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70
Q

Which monocyte relates to the recognition of antigens?

A

Langerhans cells

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71
Q

Which type of lymphocytes mature in the thymus?

A

T cells

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72
Q

Which type of lymphocyte, when in contact with APCs, matures into active helper T cells, cytotoxic T cells, or memory T cells

A

T cells

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73
Q

Which type of Lymphocyte mature in the bone marrow

A

B cells

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74
Q

Which type of lymphocyte, when on contact with antigen, activated and mature into plasma cells or memory cells

A

B cells

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75
Q

Are Natural killer cells from B cells or T cells?

A

B cells

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76
Q

Polysaccharides, polypeptides, and nucleic acids also may be what?

A

Antigenic

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77
Q

white blood cell known as the memory cell

A

lymphocytes

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78
Q

Antigen description

A
  • Provoke specific immune response when introduced into the body
  • Typically, large protein molecules are found on cell membranes/walls of microorganisms or tissues  incompatible with blood cells, vaccines, pollen, egg whites, animal dander, and insect or snake venom.
  • Antigenic determinant site (epitope) – part of the antigen that causes a specific immune response
  • Characteristics of complete antigens (immunogens)
  • Large molecules with multiple determinant sites
  • Have two characteristics: Immunogenicity – the ability to stimulate a specific immune response
  • Specific reactivity – ability to stimulate specific immune system components
  • Small molecules (e.g., dust) that cannot evoke an antigenic response alone  may link to proteins (haptens) to form complete antigens
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79
Q

When antigens are encountered in the body –> two major groups of cells generate effective immune responses which are…

A
  • Lymphocytes
  • Antigen-presenting cells (APC’s)
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80
Q

What is the primary immune response for antigens?

A
  • B cells produce antibodies to eliminate extracellular antigens
  • Antibodies react specifically to that antigen
  • Takes approximately 3 days
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81
Q

What is the secondary immune response for antigens?

A

Subsequent encounters with an antigen trigger memory cells

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82
Q

IgM desc.

A

Responsible for primary immunity
- Produced 48-72 hrs after an antigen enters body
- Does not pass through placenta

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83
Q

IgG desc

A

Major immunoglobin
- Results from secondary exposure to a foreign antigen
- Responsible for antiviral and antibacterial activity
- Passes through the placenta barrier

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84
Q

IgA desc

A

Protects mucous membranes
- Does not pass through the placenta
- Congenital deficiency are prone to autoimmune disease

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85
Q

IgD desc

A

Role unknown
- Short half-life (3 days)
- Assist in the regulation of mucosal homeostasis

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86
Q

IgE desc

A

Increases during allergic reactions, anaphylaxis
- important defense against parasitic disease

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87
Q

Intracellular pathogens —> activate ___ lymphocytes

A

T

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88
Q

Cell-mediated immunity

A
  • acts at the cellular level by attacking antigens and B cells directly
  • T lymphocytes subdivide into helper T cells or suppressor T cells
  • Helper T cells –> initiate immune response
  • Suppressor T cells limit immune response
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89
Q

Complement System desc

A
  • consists of 20 plasma proteins (complement proteins)
  • component of blood serum in an inactive form
  • Activates general inflammatory reaction  increases vascular permeability, enhances phagocytosis, and promotes vasodilation
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90
Q

Cytotoxic T lymphocytes

A
  • Attack malignant cells
  • Responsible for rejection of transplants, tissue grafts
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90
Q

Immune cells secrete cytokines
-this is crucial for controlling what?
- Cytokines carry what? and for what?

A
  • crucial in controlling the growth and activity of other immune system cells and blood cells
  • Cytokines carry messages for immune system function
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91
Q

The Lymphoid System consists of…..

A

lymph nodes, spleen, thymus, bone marrow, and lymphoid tissue

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92
Q

Why do lymphoid systems exist?

A
  • Recover proteins from the vascular system
  • Protects bloodstream from invading organism
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93
Q

The function of lymph nodes

A
  • Filter foreign products or antigens –> immune surveillance
  • Houses and supports the proliferation of lymphocytes and macrophages
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94
Q

Spleen description

A
  • Largest lymphoid organ
  • Filters blood – only lymph organ that can filter blood
  • Two kinds of tissue
  • White pulp: lymphoid proliferation, immune surveillance, B-cells
  • Red pulp: blood filtration, removes debris, and foreign matter from blood
  • Stores blood and breakdown products of RBCs for future use
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95
Q

Thymus gland description

A
  • Considered a central lymphoid organs
  • Located superior anterior mediastinal cavity beneath the sternum.
  • During fetal life and childhood, site for maturation and differentiation of thymic lymphoid cells ( after puberty begins to atrophy
  • Thymosin stimulates lymphopoiesis – formation of lymphocytes or lymphoid tissue
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96
Q

What does the bone marrow produce and store?

A

hematopoietic stem cells
- all cellular components of blood are derived from this

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96
Q

related to the spleen, what is the red pulp

A

Phagocytic cells dispose of damaged or aged RBC’s and platelets

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97
Q

What is considered the central lymphoid organs

A

Bone Marrow

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98
Q

What type of tissue is located at key sites of potential invasion by microorganisms such as the skin, submucosa of GI, Resp, and GU tracts

A

Lymphoid tissues

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99
Q

Tonsils and adenoids protect the body from what?

A

from inhaled and ingested foreign agents

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100
Q

What is lymph? (part of lymphatic system)

A

watery fluid within the lymphatic system

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101
Q

What are the 4 first lines of defense against infection

A
  • Skin
  • Mucous - line cells of body - trap microorganisms or foreign substances
  • Ciliary movements
  • Bactericidal substances in body fluids
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102
Q

A barrier breach in the skin would result in what?

A

Inflammation

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103
Q

What are the 3 reactions to inflammation; how the body processes invader?

A
  • Invader neutralized and eliminated
  • Destroyed tissue removed
  • Healing and repair initiated
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104
Q

Are children and older adults more prone to infection and why?

A

B/c older adults have declining immune function while children have an immature immune system

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105
Q

More immunity genetic considerations happen in which gender?

A

Females

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106
Q

Type 1: IgE- mediated hypersensitivity

A
  • Rapid development of symptoms after exposure to antigens  15 – 30 minutes (usually)
  • May involve skin, eyes, nasopharnyx, bronchopulmonary tissue, and GI tract
  • Can sometimes have delayed onset 10 – 12 hours
  • Most severe  anaphylaxis
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107
Q

Type II: Cytotoxic hypersensitivity description

A
  • Response is rupture of cells that are targeted by the immune response
  • Mediated by IgM or IgG antibodies
  • Examples: transfusion reactions, Rh incompatibility, Hashimoto thyroiditis
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108
Q

Type III: Immune complex-mediated hypersensitivity Description

A
  • Inflammatory response in the targeted tissues — tissue damage
  • May occur 3- 10 hours after antigen exposure
  • Autoimmune disorders such as SLE, RA
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109
Q

Type IV: Delayed-type hypersensitivity description

A
  • Characterized by tissue damage at the site of antigen contact
  • Damage occurs 24 – 48 hours after exposure
  • Examples: TB test (Mantoux test) allergic contact dermatitis
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110
Q
  • Occurs when the immune system attacks components of its own body
  • The immune system fails to distinguish itself from others.
A

autoimmune disease

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111
Q

Rheumatoid arthritis (RA), Psoriasis, Chron’s disease, Lupus (SL), scleroderma etc.
- these are all examples of what type of disease

A

Autoimmune disease

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112
Q

What are the 3 types of transplant reactions

A
  • Hyperacute Rejection
  • Acute rejection
  • Chronic Rejection
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113
Q

What is a hyperacute rejection

A
  • Occurs in minutes or hours after transplantation
  • Characterized by organ swelling, clot formation and hemorrhage
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114
Q

What is an acute rejection

A
  • Occurs in weeks after transplantation  1week to 3 months
  • Failure in function of organ and pai
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115
Q

What is a Chronic rejection

A
  • occurs months to years after transplantation
  • Slow, insidious failure occurs as a result of immune-mediated damage
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116
Q

which type or immune deficiency (primary or secondary)

Congenital
May affect T cells and/or B cells
May result from defects in WBCs

A

primary

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117
Q

which type or immune deficiency (primary or secondary)

  • Acquired later in life
  • Lead to a decrease immune function and increased susceptibility to infection and malignancies
  • Typically result from trauma and stress
  • May result from cancer therapies
  • AIDS results from HIV  attacks and depletes helper T-cells  causing immune dysfunction.
A

secondary

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118
Q

what impairs immune response when related to nutrition

A

Protein-energy malnutrition and lipid, vitamin and mineral deficiencies

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119
Q

modifiable risk factors for immunity

A
  • Weight
  • Stress
  • Alcohol, drug, cigarette use
  • IV drug use
  • Risky sexual behaviors
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120
Q

What type of vaccine is a killed virus

A
  • contained killed version of microorganism
  • induces body to produce antibodies not as strong as live virus
  • Example: inactivated poliovirus vaccine
121
Q

What type of vaccine is a toxoid vaccine

A
  • toxin from a microorganism is treated (to weaken its effects) and given to individual.

-Boosters are needed to maintain ongoing protection

  • Example: tetanus toxoid
122
Q

What type of vaccine is a live virus

A
  • contains an attenuated (weakened) form of the microorganism that causes
    a disease.
  • Examples: measles and varicella
123
Q

What type of vaccine is a recombinant vaccine

A
  • DNA from two or more sources is combined to genetically alter an organism
  • Examples: Hepatitis B, HPV, and Acellular Pertussis
  • Boosters are typically required
124
Q

What type of vaccine is a conjugated virus

A
  • A combination of a weak antigen joined with a strong antigen as the carrier to increase the immune response to the weaker antigen
125
Q

What reaction is rare when getting a vaccine?

A

Anaphylaxis

126
Q

Vaccine hesitancy description

A
  • Concerns about overloading immune system at young age, vaccine safety, religious beliefs and personal experiences
  • Belief in “herd immunity” will protect their child so no need to vaccinate
  • Belief that natural healing methods are better than vaccines
  • Doubts about the effectiveness of vaccines

-Perceived associations between vaccines and development of chronic disease

127
Q

What should healthcare provider offer to a patient that has vaccine hesitancy

A
  • Provide balanced information about risks and benefits

-Legislation requiring informed consent varies from state to state

128
Q

What is the nurse’s responsibility to a patient with vaccine hesitancy

A

Informing parents/guardian
Supplying literature
Obtaining written consent

129
Q

12 diagnostic tests related to immunity

A

Enzyme immunoassay (EIA)
Enzyme-linked immunosorbent assay (ELISA)
Antinuclear antibody (ANA)
Autoantibody
Immunoglobulins
Polymerase chain reaction (PCR)
Rapid HIV tests
Radioallergosorbent test (RAST)
Skin reactions
Western blot test
Complete blood count (CBC)
Complement

130
Q

Independent interventions related to immunity

A

Proper nutrition
Adequate exercise
Sleep
Stress reduction
Stress management

131
Q

lifespan considerations for Infants and Children related to immunity

A
  • Immune system development influenced by early in utero experiences, environmental exposures after birth, other factors
  • IgG: only immunoglobulin crosses placenta
    Maternal IgG disappears by 6–8 months
  • Child’s IgG increases gradually until 7–8 years Cell-mediated immunity achieves full function early in life
  • Premature newborns most prone to infection
132
Q

lifespan considerations for Adolescents related to immunity

A
  • Immune system still maturing
  • Long-term damage from marijuana use chronic inflammatory, autoimmune response
133
Q

lifespan considerations for Pregnant Women related to immunity

A
  • Brief decline in maternal cell-mediated immunity during pregnancy
  • Prevents rejection of fetus
  • Mother at greater risk of developing viral, bacterial infections
  • Be up-to-date on immunizations before pregnancy
  • May get immunizations during pregnancy if needed except live viruses*
134
Q

lifespan considerations for Older Adults related to immunity

A
  • Normal changes associated with aging
  • Decrease in immune response
  • Lower resistance to infection
  • Poor response to immunizations
  • Immune system changes may bring on insulin resistance
  • Hypersensitivity response reduced or delayed
  • Autoantibodies more common
135
Q

What is the cause of neutrophilia?

A
  • Acute infection or stress response, myelocytic leukemia, inflammatory or metabolic disorders, tissue necrosis
136
Q

What is the cause of eosinophilia?

A

parasitic infections, allergic reactions, autoimmune disorders

137
Q

What is the cause of Basophilia

A

– hypersensitivity responses, leukemia, splenectomy, hypothyroidism

138
Q

What is the cause of monocytosis?

A

– chronic inflammatory disorders, infections, leukemia, Hodgkin disease

139
Q

What is the cause of lymphocytosis?

A

– infections, viral infections, lymphocytic leukemia

140
Q

Related to inflammation, what is pharmacological therapy aiming to do?

A
  • Aimed at reducing inflammatory response and the symptoms of pain and fever associated with inflammation
  • Salicylates - ASA
  • Nonopioid Analgesics – Acetaminophen
  • NSAIDS -
  • Corticosteroids – treat autoimmune disease
  • Can increase glucose, cause electrolyte imbalance, weight gain, nausea, impair wound healing
141
Q

Chronic inflammatory state is associated with ___ and ______

A

age and obesity

142
Q

Most anti-inflammatory drugs act to decrease prostaglandins which promotes ________.

A

permeability

143
Q

What is hepatitis

A

inflammation of the liver

144
Q

What does hepatitis do to liver

A

prevents the liver from functioning

145
Q

the liver is responsible for the production and processing of what?

A
  • Production of bile to aid in breakdown and absorption of fats
  • Processes nutrients that are carried from the small intestines via blood
146
Q

Why younger children at risk with inflammation?

A

their structure is smaller such as short epiglottis, shorter and narrower trachea

147
Q

lifespan considerations for pregnant women related to inflammation

A
  • Immune system is diminished as protection for the fetus
  • Pre-eclampsia – thought to be an inflammatory mediated hypertensive disorder of pregnancy
  • Changes in immune system can lead to hypersensitivity to nonpathogenic stimuli and can lead to development of chronic inflammatory disease.
148
Q

Lifespan considerations for older adults related to inflammation?

A
  • Inflammatory markers – C reactive protein etc. may be increased in older and obese individuals
  • Increase markers are seen in increased fragility of the individual
  • Increase in markers is also associated with increased morbidity, comorbid conditions and more frequent hospitalization
  • Can reduce inflammation through diet and resistance training
149
Q

pathophysiology of hepatitis

A
  1. inflammation damages hepatic cells and disrupts liver function
    1a. cell-mediated immune responses damage hepatocytes and Kupffer cells (Hyperplasia, necrosis and cellular regeneration)
  2. Biliary flow of bile ducts may be obstructed by the inflammatory process (causing jaundice)

Mild: (Hep A)
- liver parenchyma is not significantly damaged

Severe: (Hep A &/or Hep C)
- severe liver damage
- Infiltration by lymphocytes, macrophages and other WBC’s causes inflammation that block drainage
- Structural changes occur in parenchymal cells – altered liver function
- Impaired bile secretion
- Elevated ALT and alkaline phosphatase levels
- Decrease albumin systhesis
- There is a disruption of metabolism of nutrients, drugs, alcohol and toxins and bile elimination

150
Q

How is Hepatitis A transmitted?

A

fecal-oral, rare complications, vaccine

151
Q

How is Hepatitis B transmitted?

A

blood and body fluids, perinatal, complications: chronic hepatitis, cirrhosis, liver cancer, vaccine

152
Q

How is Hepatitis C transmitted?

A

blood and body fluids, perinatal, complications: chronic hepatitis, cirrhosis, liver cancer

153
Q

How is Hepatitis D transmitted?

A

blood and body fluids, perinatal, rare, complications chronic hepatitis, liver cancer, fulminant hepatitis

154
Q

How is Hepatitis E transmitted?

A

– fecal-oral, complications: chronic hepatitis, fulminant hepatitis, may be severe in pregnant women

  • Effects may be local within the liver or systemic
155
Q

what are 2 nonviral forms of hepatitis?

A

Alcoholic and drug induced hepatitis

156
Q

What are the disease states of Hepatitis?

A
  • Autoimmune hepatitis
  • Metabolic-disorder hepatitis
  • Nonalcoholic fatty liver disease (occurs in pts w/diabetes or obesity)
157
Q

Non-viral risk factors for hepatitis

A
  • Autoimmune disorders such as systemic lupus erythematous
  • Alcoholism
  • Obesity
  • Diabetes
  • Medication such as high doses of Tylenol
  • Toxins including poisonous mushrooms and vinyl chloride
158
Q

tips for prevention of Hepatitis

A
  • Healthy lifestyle choices
  • Avoid toxins, chemicals and medications causing hepatitis
159
Q

Risk factors for getting Hepatitis A

A
  • Contaminate food and water (most common cause)
  • Travel in areas with high rates
  • HIV-positive status
  • Living with an individual who has
  • Illicit drug use (any form)
  • Male to male sexual contact
160
Q

How to prevent Hepatitis A

A
  • Vaccination – 2 available
  • Practice good hand hygiene
  • Boil water or use bottle water, cook foods thoroughly and peel raw vegetables – when traveling in developing countries
161
Q

Risk factors for Hepatitis B

A
  • Sexual contact with contaminated blood or body fluids (most common cause)
  • Multiple sexual partner
  • Male to male sexual contact
  • Sharing of IV needles
  • EXPOSURE TO BLOOD ***
  • Living with someone infected
  • Hemodialysis
  • Traveling to areas with high rates
162
Q

How to prevent Hepatitis B

A
  • Vaccination
  • Practice safe sex
  • Avoid sharing personal items (razors, toothbrush, needles)
163
Q

Risk factors for Hepatitis C

A
  • Contact with infected blood (sharing of needles most common causes)
  • Healthcare worker exposure to infected blood
  • Illicit drug use (injections)
  • History of HIV
  • Boy piercing or tattoo with infected equipment
  • Having received blood products before 1987
164
Q

Prevention for Hepatitis C

A
  • Practice safe sex
  • Avoid sharing personal items (razors, toothbrush, needles
165
Q

Risk factors for Hepatitis D

A
  • Illicit drug use (injections)
  • Having HBV
  • Male to male sexual contact
  • Multiple blood transfusion
  • Get the HBV vaccine
166
Q

Risk factors for Hepatitis E

A

Drinking contaminated water

167
Q

Prevention of Hepatitis E

A
  • Practice good hand hygiene
  • When traveling in developing countries, boil water or use bottle water, cook food thoroughly and peel raw fruits and vegetables.
168
Q

What are the clinical manifestations (S&S) of acute hepatitis

A

Acute hepatitis – asymptomatic during incubation period

  • No symptoms if mild
  • Fever
  • Malaise and fatigue
  • Jaundice
  • Pruritus
  • Abdominal pain in RUQ or epigastric area
  • Anorexia
  • N/V
  • Myalgia and arthralgia
169
Q

What are clinical therapies

A
  • Supportive therapy including rest, nutrition, vitamin supplements and avoidance of alcohol
170
Q

what is myalgia

A

pain in muscles

171
Q

what is arthralgia

A

pain in joints

172
Q

What are the clinical manifestations (S&S) of chronic hepatitis

A
  • No symptoms if mild
  • Malaise and fatigue
  • Arthralgia
  • RUQ abdominal pain or pressure from the enlarged liver
  • Jaundice
173
Q

What are the clinical therapies to help resolve chronic hepatitis

A
  • Supportive therapy for lifelong management
  • Interferons and antiviral medications
  • Liver transplantation if liver failure occurs
174
Q

What is the prodromal phase?

A
  • occurs between exposure to virus and appearance of clinical manifestations
    • jaundice - d/t inc. bilirubin in blood
  • starts about 2 weeks after exposure can be insidious or rapid in onset
  • symptoms:
  • Frequent episodes of myalgia and arthralgia
  • Anorexia
  • Mild but chronic abdominal pain in RUQ or epigastrium
  • Low-grade fever
175
Q

What is the Icteric Phase?

A
  • Begins with onset of jaundice (some patients may not experience)
  • Approximately 5 – 10 days after initial symptoms
  • Dark colored urine – d/t increased levels of conjugated bilirubin (results from breakdown of hemoglobin conjugated by hepatocytes and excreted in the bile.
176
Q

What is the Convalescent Phase (recovery)?

A
  • Increase sense of well-being usually following 2-3 weeks of acute illness
  • Disappearance of abdominal pain and jauncie
  • Increase levels of energy
  • Improved appetite
  • HAV - resolves in < 2 months but can last as long as 6 months
  • HBV – may take up to 6 months
177
Q

What does ALT stand for

A

alanine aminotransferase

178
Q

What does ALP stand for

A

alkaline phosphatase

179
Q

What deos LDH stand for

A

lactic dehydrogenase

180
Q

What does AST stand for?

A

aspartate aminotransferase

181
Q

What are the 7 types of diagnostic tests for Hepatitis

A

ALT, ALP, LDH, AST, GGT, serum bilirubin and liver biopsy

182
Q

lifespan considerations in Infants and Children related to hepatitis

A
  • Hep A most common spread at daycare centers where children are in diapers and being potty trained
  • Hep B spread by infected mothers to children – dependent on viral load
  • Young asymptomatic - adolescents may have more severe symptoms
  • Hep C – spread through vertical transmission to children (or exposure blood and fluids)
  • Hep D and E less common – HDV only occurs In presence of HBV – rarely seen in children born in US d/t vaccination in infancy
  • Acute hepatitis onset usually rapid – fever, N/V, decrease appetite, sore muscles stool may appear clay-colored and urine dark. Jaundice at later stages
183
Q

lifespan considerations in Pregnant women related to hepatitis

A
  • Flulike symptoms with jaundice more severe during pregnancy
  • Lab tests to differentiate pregnancy complications – preeclampsia
  • Hep B and C can pass to babies during birth
  • Hep B vaccination after birth can decrease likelihood of HBV infection
  • Women with hep B – babies should receive HBV immune globin within 12 hours after birth followed up with 2-3 additional vaccinations over 15 months
  • Can breastfeed an infant who has been vaccinated
  • All pregnant women are tested for HBV in pregnancy to prevent vertical transmission
184
Q

lifespan considerations in older adults related to hepatitis

A
  • Complications are higher in older adults
  • Morbidity higher d/t diminished immune response, nutritional deficiencies and cumulative toxin exposure
  • Acute HAV clinically severe and more likely to experience complications
  • Acute HBV tends to be asymptomatic and there is a higher progression rate to chronic HBV
  • HCV most frequent cause of acute hepatitis in age group
    - experience more complications of cirrhosis
    - scar tissue formation is more rapid
  • Hep D and E may occur but less prevalent
  • Antiviral therapy contraindicated in many older adults with HCV d/t age and other medical conditions
  • Direct Acting Antiviral Agents have been effective in treating adults > 65 years old
  • Encourage vaccination
185
Q

What is an infection?

A

An invasion of body tissue by microorganisms with the potential to cause illness or disease

186
Q

What is the major defense mechanism of the body related to infection?

A

the immune system

187
Q

what is a disease without recognizable findings? (Microorganism is detected but little to no symptoms seen) – can cause considerable damage example CMV infection in women can lead to significant disease in unborn children.

A

subclinical disease

188
Q

an illness that directly passes from one individual/animal to another by contact with bodily fluids or indirectly by contact with contaminated objects, airborne particles, or vectors.

A

a communicable disease

189
Q

any communicable disease caused by microorganisms that are commonly transmitted from one individual or animal to another or from an animal to an individual.

A

an infectious disease

190
Q

what is a pathogen?

A

microorganism that causes disease

191
Q

a type of pathogen that causes disease only in susceptible individual
Examples: individuals with Cancer or HIV

A

opportunistic pathogen

192
Q

what are mycoplasma bacteria?

A

small, no cell wall, resistant to antibiotics that inhibit cell wall synthesis (penicillin)

193
Q

What is colonization?

A

The process by which microorganisms become resident flora

They grow and multiply but do not cause disease

194
Q

What is a local infection?

A

Limited to a specific area of the body
Example: Otitis media, UTI

195
Q

What is a systemic infection

A

Infection spreads and affect different parts of the body
Example: cellulitis or sepsis

196
Q

what is bacteremia (systemic infection)

A

when a culture of blood reveals a bacteria

197
Q

What is septicemia (systemic infection)

A

when bacteremia results in a systemic infection

198
Q

what is asepsis

A

absence of disease-causing microorganism

199
Q

What is the aseptic technique?

A

decrease possibility of transferring microorganisms

200
Q

medical vs surgical asepsis

A

Medical asepsis – practices that intend to confine specific microorganisms to specific areas – limiting the number, growth, and transmission of

  • Referred to as “clean” – almost all microorganisms are absent
  • “Dirty” or soiled, contaminated - microorganisms are likely to be present

Surgical asepsis (aka sterile technique) - practices that keep an area or object free of all microorganisms.
- Includes practices that not only destroy microorganisms but also spores

201
Q

What is an etiologic agent (infectious agent)

A

Dependent on number of microorganisms present, virulence, and pathogenicity, ability to enter body, susceptibility of host and the ability to live in host body

202
Q

What is a reservoir

A

Source of microorganism – can be from another part of body, other humans, plants, animals and environment. Also food, water and feces can be a reservoir

203
Q

What is the portal of exit?

A

Respiratory tract, GI tract, Urinary tract, Reproductive tract, Blood and Tissue

204
Q

What is the Method (Or means) of transmission

A
  • Direct transmission – touching, biting, kissing, or sexual intercourse. Droplet is considered direct but within 3 feet of each other (sneezing, coughing, spitting, singing, or talking)
  • Indirect transmission - (vehicle-borne or vector-borne)
  • Airborne transmission – transmission of droplets or dust, transmitted by air currents (TB, C-diff spores)
205
Q

what is a Portal of entry

A

Where enters body - respiratory, break in skin barrier, genitalia , urethral meatus

206
Q

What is a susceptible host?

A

Anyone at risk for infection (those individuals who do not have antibodies, a compromised host – very young, very old, immunosuppressive treatment for Cancer or chronic illnesses)

207
Q

how are nasal passages barriers to infection

A

they trap microorganisms, dust, and foreign materials in the cilia and moist mucous membranes

208
Q

How are lung barriers to infection

A

they are equipped with alveolar macrophages that ingest microorganisms, other cells, and foreign particles

209
Q

How is the vagina a barrier to infection

A

they have a low pH which inhibits the growth of disease-producing organisms

210
Q

does saliva help with preventing infection?

A

yes, it is a barrier

211
Q

related to infection, what is a specific defense?

A
  • Immune system when an antigen induces a state of sensitivity and antibodies respond to contain or destroy the antigen
212
Q

what lack of help to facilitate transmission of disease; very common in children

A

Poor hand hygiene

213
Q

What are the factors that facilitate transmission of infection?

A
  • organism’s resistance to drying and variations in environmental temperature
  • the ability to alter/destroy the normal function of the host cell and promote colonization, proliferation, and invasion by the pathogen
  • adhesion factors produced by or incorporated into the cell wall to improve its ability to attach to or colonize the host
  • toxin production
  • endotoxin
  • blocking specific immune responses
214
Q

what is an endotoxin?

A

found in the cell wall of gram-negative bacteria and are released only when the cell is disrupted
- can activate many regulatory systems and cause fever, inflammation, clotting, bleeding or hypotension when released in large quantities

215
Q

what is an exotoxin?

A
  • soluble proteins that the microorganism secrete into surrounding tissue
  • Highly poisonous and can cause cell death or dysfunction
216
Q

a therapy we can give to help with infection, and/or inflammation would be to give….

A

fluids

217
Q

if patient has breathing difficulties, a therapeutic intervention that would be recommended is giving what??

A

Fluid, fluid, fluid

218
Q

what are the 4 stages of the infectious process?

A
  • incubation period
  • prodromal stage
  • illness stage
  • convalescent stage
219
Q

what is the incubation period?

A
  • Pathogen begins active replication but does not cause symptoms
  • May last from hours to years (salmonella – HIV)
220
Q

what is the prodromal stage?

A
  • Symptoms begin to appear
  • Usually nonspecific symptoms - general malaise, fever, myalgias, headache, and fatigue.
221
Q

What is the illness stage?

A
  • Pathogen proliferates and disseminates rapidly
  • Toxic by-products of microorganism metabolism and cell lysis occur
  • Immune response
  • Above Produces tissue damage and inflammation
  • Fever chills may be significant * elderly and patients with ETOH abuse may have hypothermia
  • Tachycardia and Tachypnea d/t increase metabolic demand
  • Localized manifestations: erythema, heat, swelling, pain, and impaired function (if internal organs, may experience tenderness to palpation over the site or show signs of impaired function (example: renal infection - -hematuria and proteinuria)
222
Q

What is the convalescent stage?

A
  • The infection is contained, and the pathogen is eliminated
  • Affected tissue is repaired and manifestations are resolved.
223
Q

What is an Iatrogenic infection

A

(Healthcare-associated infection [HAI])
- result of a diagnostic or therapeutic procedure

224
Q

what is a compromised host

A

(Healthcare-associated infection [HAI])

body defenses have been lowered d/t surgery or illness

225
Q

what is a “immunological responses decreased”

A

(Healthcare-associated infection [HAI]) patient is more prone to HAI d/t Cancer, chronic disease, pressure ulcers or organ transplants

226
Q

what is the result of antibiotic therapty

A

(Healthcare-associated infection [HAI])
alteration of body’s natural flora

227
Q

What invasive procedures can result in an HAI?

A

Catherization: Urinary, cardiac, insertion of IV
- Organisms infected this way may be resistant to drugs and not respond to antibiotics

228
Q

What is the most simple mistake that can cause an HAI?

A

poor hand hygiene

229
Q

is urinary catheterization the #1 cause of HAI?

A

Yes

230
Q

How does a patient get healthcare-associated pneumonia

A

When patient is put on a ventilator, tracheostomies, endotracheal intubation
- put on a VAP

231
Q

What is the most common HAI (the most common infection?)

A

UTI

232
Q

Why are antibiotic-resistant bacteria increasing?

A

bc of inappropriate or prolonged use of antibiotics

233
Q

Where does MRSA colonize?

A

In nares and skin

234
Q

How is MRSA transmitted?

A

Transmitted primarily by direct physical contact not through respiratory droplets

235
Q

Integumentary system includes what 4 things

A
  • Skin
  • hair
    nails
  • Sebaceous sweat, and mammary glands
236
Q

Functions of the skin

A
  • protects underlying tissues
  • nerves in skin enable perception
    This includes:
  • touch
  • pain
  • pressure
  • heat
  • cold
  • body temp regulation
237
Q

What helps protect skin from UV damage

A

Melanin

238
Q

What are internal factors of the appearance of the skin

A
  • Genetics
  • Age
  • Individual’s underlying health
239
Q

What are the external factors of the appearance of the skin?

A
  • Activity
240
Q

For skin disorders, what is the most diverse collection of disorders

A

Infectious disorders

241
Q

What is contact dermatitis

A

inflammatory disorder of the skin

242
Q

What is an irritant for contact dermatitis?

A

Contact with chemicals, soaps, dyes, detergents, metals, perfumes

243
Q

What are the symptoms for a characterized by damage to dermis, epidermis?

A
  • Red, pruritic rash where skin came into contact with allergen or irritant
244
Q

What causes inflammatory skin disorders?

A
  • Exposure to environmental stressors
  • Injury to skin
245
Q

What is an observable changes form normal skin structure

A

Lesions

246
Q

For skin disorders, what is the primary inflammatory skin disorder response?

A
  • Arise from previously healthy skin
  • Macules, patches, papules, nodules, tumors, vesicles, pustules, bullae, wheals
247
Q

For skin disorders, what is the secondary inflammatory skin disorder response?

A
  • Results from a change in primary lesions
  • Crusts, scales, lichenification, scars, keloids, excoriation, fissure, erosion, ulcers
248
Q

What is an intentional wound

A

Occurs during therapy such as operation or venipuncture

249
Q

What is an unintentional wound?
- What is a closed wound?
- what is an open wound?

A
  • Accidental such as fracture
  • Closed: tissues traumatized without break in skin
  • Open: Skin or mucous membrane surface is broken
250
Q

What are the degrees of contamination for wounds?

A
  • Celan wounds
  • Clean contaminated wounds
  • Contaminated wounds
  • Dirty, infected wounds
251
Q

What is a partial thickness wounds

A
  • Confined to skin
  • Heal by regeneration
252
Q

What is a full-thickness wound?

A
  • Involve dermis, epidermis, subq tissue, possibly muscle and bone
  • Require connective tissue repair
253
Q

What are the most common skin disorders

A
  • acne
  • dermatitis
  • Inflammatory reactions to topical drugs
  • Infectious diseases of skin
254
Q

What is the most common form of cancer

A

skin

255
Q

inheritable skin disorders

A
  • epidermolysis bullosa
  • ichthyosis
  • albinism
256
Q

are men more affected by infection skin disorders

A

yes

257
Q

are men more affected by pigmentary, autoimmune disorders?

A

no, women are

258
Q

When ou age, what hapens to your skin

A
  • change in skin thickness
  • Surface pH
  • quality of wound healing
259
Q

Is lighter skin more prevalent in individuals for some conditions

A

no, some conditions are more prevalent in individuals with darker skin as some more prevalent in lighter skin

260
Q

What are modifiable risk factors for the skin

A
  • proper skin care
  • avoid irritants or allergens
  • avoid excessive cleansing of the skin
  • what medications that cause thinning fot he skin
  • watch nutrition
261
Q

What types of screenings should be done for the skin

A
  • regular self-examination
  • develop familiarities with one’s skin
    – professional examinations
262
Q

How to prevent skin disorders

A
  • bathing/grooming/cleansing
  • use lubricants/lotion
  • promote hydration
  • avoid alcohol
263
Q

The oral activity is susceptible to injury to what?

A

to injury of the lips, soft tissues, buccal cavity, and/or oropharynx, which may compromise health and create wounds

264
Q

What are the goals of treatment of independent interventions for patient?

A
  • Control severity
  • Prevent infection
  • Promote healing
265
Q

inter-professional teams improve patient outcomes such as who?

A
  • Nurses
  • nurse care managers
  • attending healthcare provider
  • oncologists
  • yada yada….
266
Q

When do we use OTC medications for skin issues

A

For less serious conditions such as:
- sunburn
- acne
- most are topical

267
Q

Examples of extensive or long-term prescription therapy

A
  • Eczema, dermatitis, psoriasis
  • can be oral or topical
  • under doctors supervision
268
Q

what situations puts you at risk for skin breakdown?

A
  • poor blood circulation
  • fluid deficit/excess
  • impaired mobility
  • impaired sensation
  • malnutrition
  • overweight
  • skin diseases
269
Q

Lifespan consideration for newborns on tissue integrity

A
  • Skin covered by vernix caseosa in utero

Skin conditions that may be present at birth:
- Milia
- mild acne
- erythema toxicum
- “stork bites”

270
Q

Lifespan consideration for Children on tissue integrity

A
  • Larger Body surface area + thinner skin

More commonly affected by viral infections

271
Q

Lifespan consideration for Adolescence on tissue integrity

A
  • skin goes under hormonal changes
  • in females, can cause premenstrual exacerbation of preexisting skin disorders

skin disorders that tend to appear in adolescence:
- acne
- seborrheic dermatitis
- psoriasis
- tinea versicolor

272
Q

Lifespan consideration for Pregnant women on tissue integrity

A
  • skin changes related to hormonal increases in pregnancy such as:
  • hyperpigmentation
  • stretch marks (striae distensae)
  • Pruritis gravidum
  • possible atopic eruption of pregnancy (in roughly 50% of pregnancies
273
Q

Lifespan consideration for Older adults on tissue integrity

A

Normal skin changes in the aging process
- occurs slowly
- glands decrease oil production

274
Q

What is primary intention healing?

A
  • tissue surfaces have been approx. (closed) with little or no loss
  • Formation of minimal granulation tissue, scarring
275
Q

What is secondary intention healing

A
  • Extensive wound with tissue loss and edges that cannot or should not be approx.
  • Differs from primary intention healing
  • Repair time longer
  • Scarring greater
  • Susceptibility to infection greater
276
Q

What is tertiary healing

A
  • Wound left open for 3-5 days, then closed
  • Allows edema of infection to resolve, wound to drain
277
Q

What is the inflammatory phase

A
  • first 3-6 days after injury

Hemostasis results from
* Vasoconstriction
* Retraction of injured blood vessels
* Deposition of fibrin
* Formation of blood clots
* Formation of scab on surface of wound

278
Q

Inflammatory phase: what are Phagocytosis

A
  • Macrophages
  • Engulf microorganisms and cellular debris
  • Secrete angiogenesis factor: stimulates formation of epithelial buds at end of injured blood vessels
  • This microcirculatory system sustains healing process
279
Q

What is the Proliferative phase

A

Proliferative phase — day 3- 4 to about day 21
* Fibroblasts begin to synthesize collagen
* If wound is sutured, a raised “healing ridge”
appears under suture line
* Capillaries grow across the wound,
increasing blood supply
* Fibroblasts deposit fibrin in the wound

Granulation tissue
* Translucent red tissue, fragile, bleeds
easily
* When edges of wound not sutured, area
must be filled with granulation tissue
* When tissue matures, marginal epithelial
cells migrate to it, proliferating to fill
wound
* If wound does not close by epithelialization,
scab forms
* Later, if wounds not covered by epithelial

280
Q

What is the maturation phase

A

Day 21 to 1-2 years

  • Fibroblasts continue to synthesize
    collagen
  • Collagen fibers reorganize into more
    orderly structure
  • Wound site is remodeled, contracted
  • Scar becomes stronger
  • Repaired area never as strong as
    original tissue
  • Keloid: hypertrophic scar caused by
    abnormal amount of collagen
  • Particularly in dark-skinned
    individuals
281
Q

Risk factors for complications

A

Hemorrhage
* Massive bleeding
* Hematoma: internal hemorrhage
* Risk greatest during first 48 hours after surgery
* Emergency

Infection
* Contamination of wound surface with microorganisms is
inevitable
* Presence can impair wound healing, lead to infection
* Immunocompromised patients especially susceptible
* Wound can be infected
* At time of injury
* During surgery
* Postoperatively: becomes apparent 2–11 days
postoperatively

282
Q

What is dehiscence

A

Partial or total rupture of a sutured wound

283
Q

What is evisceration

A

Protrusion of internal viscera through incision

284
Q

What are risk factors for wound healing

A
  • Obesity
  • Poor nutrition
  • Multiple trauma
  • Failure of suturing
  • Excessive coughing
  • Vomiting
  • Dehydration
  • Sudden straining may precede dehiscence
  • Wound should be supported quickly by large sterile
    saline-soaked dressings
285
Q

What is the health promotion or wound healing?

A
  • Nutrition
  • Lifestyle
  • Medications
286
Q

What areas some clinical manifestations of wounds?

A

Exudate
- Material that has escaped from blood vessels during inflammatory
process
* Deposited in tissue or on tissue surfaces

287
Q

What are the 3 types of exudate?

A
  • Serous – mild inflammation (clear or straw color)
    thin and watery
  • Purulent – thicker composed of cells and necrotic
    tissue (opaque or milky, color blue, green, yellow)
  • Sanguineous – large number of RBC’s indicates damage to
    capillaries – frequently seen in open wounds
288
Q

What is mixed exudate?

A

clear and blood-tinged drainage
* Serosanguineous: commonly seen in surgical incisions
* Purosanguineous – pus and blood – seen in a new wound that is
infected

289
Q

what are the 7 principles of wound healing to remember

A

❖ Intact skin-first line of defense against microorganisms.
❖ Careful hand hygiene is used in caring for a wound.
❖ Reposition every 2 hours to prevent skin breakdown.
❖ Adequate blood supply is essential for normal body
response to injury.
❖ Normal healing is promoted when the wound is free of
foreign material.
❖ The extent of damage and the person’s state of health
affect wound healing.
❖ Response to wound is more effective if proper nutrition is
maintained.

290
Q

Systemic factors that may affect
wound healing to remember

A

❖ Age: children and healthy adults heal more rapidly
❖ Circulation and oxygenation: adequate blood flow is essential
❖ Nutritional status: healing requires adequate nutrition
❖ Wound etiology: specific condition of the wound affects healing-necrotic
tissue or slough
❖ Health status: corticosteroid drugs and postoperative radiation therapy
delay healing, comorbidities
❖ Immunosuppression
❖ Medication use
❖ Adherence to treatment plan
❖ The more factors affecting healing increases complexity

291
Q

Local Factors that may affect
wound healing to remember

A

 Pressure-lack of blood flow
 Desiccation-too dry, cells dry up
 Maceration-too moist, promotes bacterial growth
 Trauma
 Edema-limits blood supple to the area
 Infection-leaves body is busy fighting infection, can’t heal
 Excessive bleeding-breeding ground for infection, interferes
with oxygen perfusion
 Necrosis-dead tissue
 Biofilm-thick, protective slimy barrier of sugars and proteins

292
Q

What are the 2 priorities when it comes to wound healing?

A
  • Promotion of healing
  • Prevention of Infection
293
Q

What is escharotomy done?

A

For full-thickness wounds that encircle or near encircle a body part and have formed eschar

294
Q

What pharmacologic therapy do we use for normal wound healing?

A
  • Antibacterial ointments
  • Prophylactic antibiotics
  • Analgesics
  • Complementary therapies: products containing aloe vera
295
Q

What pharmacologic therapy do we use for impaired wound healing?

A
  • Antibiotics specific to causative organism
  • In some cases, growth factors
  • Opioids, nonsteroidal anti-inflammatory drugs (NSAIDs) for
    pain management
296
Q

For non-pharmacologic therapy, what do we use for wounds with impaired healing?

A

Vacuum-assisted closure
- do not use on wounds with eschar, necrotic tissue, or malignancy present
- wounds with anything exposed

297
Q

What are 2 cellular therapies for wound healing?

A
  • Stem cell therapies
  • Skin or tissue grafts
298
Q

What does biosurgery use

A

sterile maggots

299
Q

Lifespan considerations for Newborns, infants, and children

A
  • skin more fragile and thin
  • susceptible to infection
  • major infections: Staph, Fungi
    When cleaning wounds: clean w/warm soapy water; cover with sterile bandage
300
Q

Lifespan considerations for Older Adults

A
  • Skin is more fragile
  • Hold wrinkled skin taut
  • check routinely for skin breakdown every 2 hours
301
Q

Description of an arterial ulcer

A

 Toes and feet, shin
 Deep ulcer, pale
 Shiny skin
 Loss of hair
 Pallor upon elevation
 Cool to touch
 Little to no edema
 Intermittent, severe, resting pain
 Decreased, absent pulses

302
Q

Description of a Venous Ulcer

A

 Usually around ankle
 Superficial, pink, beefy, irregular edges
 Skin looks leathery, brown, purple, dermatitis
present
 Edema present
 Aching, mild pain
 Normal pedal pulse

303
Q

Risk factors for a Diabetic Ulcer

A

 Dx of DM
 DM not well controlled
 Overweight
 Neuropathy
 Poor circulation
 Wearing poor fitting shoes
 Walking barefoot
 ETOH/smoking
 High cholesterol
 Aging
 *Often results in amputation (toe, foot

304
Q
A