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MD 4910 NCP I > 4910:C9 Cellular & Physiological Response to Injury: The Role of the Immune System > Flashcards

4910:C9 Cellular & Physiological Response to Injury: The Role of the Immune System Flashcards

1
Q

pathology

A

The study of loss of function or the changes within an organ, or organ system that occurs as a result of disease or injury.

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2
Q

pathogenesis

A

The clinical course of disease

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3
Q

idiopathic

A

unknown cause

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4
Q

iatrogenic

A

an adverse condition in a patient resulting from treatment, usually from a physician.

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5
Q

epidemiology

A

the study of rates of disease within a population; also, study of cause and distribution; focuses on outcome, morbidity & mortality, risk factors

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6
Q

incidence

A

rate or occurrence of disease, the number of new cases in a specific time period.

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7
Q

prevalence

A

total number of cases at one specific time period.

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8
Q

sequelae

A

any abnormal bodily condition or disease related to or arising from a pre-existing disease, any complication of a disease; outcome

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9
Q

prognosis

A

a prediction of the probable course and outcome of a disease, including expected response to treatment.

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10
Q

morbidity

A

the state of being diseased, disease occurrence

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11
Q

mortality

A

the incidence of death in a population associated with a particular disease

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12
Q

atrophy

A

reduction in size of muscle cells; wasting of body tissue that occurs from disuse, disease, or malnutrition. caused by decreased workload, loss of innervation, diminished blood supply, inadequate nutrition, loss of endocrine stimulation, aging

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13
Q

hypertrophy

A

increase in cell size; can be physiologic, or pathologic; may be due to increase in cell organelles, or proteins & DNA; occurs in cells that do not under go mitosis. caused by functional demand, hormonal stimulation

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14
Q

hyperplasia

A

increased number of cells; can be physiologic or pathologic; often occurs along with hypertrophy;

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15
Q

metaplasia

A

replacement of one cell type with another; often reversible & due to hostile environment; ex vit. A deficiency. caused by genetic reprograming of cells. Often precursor to cancer.

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16
Q

dysplasia

A

abnormal cell growth; ex. increase in nuclei, or rate of replication. Generally pre-cancerous.

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17
Q

neoplasia

A

growth of new tissue which is uncoordinated with that of normal tissue; can be benign or malignant

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18
Q

ischemia

A

inadequate supply of oxygen due to vasoconstriction, or blockage

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19
Q

hypoxia

A

inadequate supply of oxygen in the blood

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20
Q

infarction

A

cellular necrosis as a result of lack of oxygen

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21
Q

disease

A

process that disrupts physiologic function; homeostasis cannot be maintained; has characteristic sigs and symptoms

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22
Q

disease process

A

epidemiology, etiology, pathophysiology, clinical manifestations, outcome

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23
Q

etiology

A

the cause of a disease; genetic, acquired, multifactorial, idiopathic, iatrogenic

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24
Q

causes of cellular injury

A

deficiency, intoxication, trauma, infection

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25
Q

How can cell injury be monitored?

A

functional loss, release of cell constituents, electrical activity, biopsy; changes can be measured in the blood

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26
Q

intoxication

A

a cause of cellular injury which can be either exogenous, or endogenous

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27
Q

dyspnea

A

difficulty breathing

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28
Q

hyaline

A

a cellular response to disease or damage; deposition of collagen, fibrin, & amyloid within & between cells.

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29
Q

Standard Precautions

A

Set of guidelines developed by the CDC, include all personal and environmental procedures that should be followed to prevent transmission of infection.

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30
Q

course of an infection

A

incubation, prodromal, acute period, recovery/convalescence

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31
Q

incubation period

A

time between entry & appearance of clinical signs

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32
Q

prodromal period

A

individual begins to experience vague symptoms

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33
Q

myeloid stem cells

A

become monocytes & macrophages, and megakaryocytic, granulocyte, RBCs, monocytes, PMNs

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34
Q

Granulocytes

A

aka. polymorphonuclear leukocytes: basophil, eosinophil, neutrophils.

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35
Q

polymorphonuclear leukocytes

A

a category of WBCs which includes: neutrophils, eosinophils, & basophils.

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36
Q

neutrophil

A

a PMN, major cell recruited to ingest, kill, & digest pathogen; first cell to inflammatory response; remove cellular debris

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37
Q

eosinophils

A

a PMN, defend against parasites; participate in common hypersensitivity (allergic) reactions; are phagocytic, but primarily produce chemicals to combat helminths.

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38
Q

basophil

A

a PMN; produce cytokines that help defend against parasites; produce histamine and serotonin involved in allergic response; promote vasodilation

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39
Q

natural killer cells

A

from lymphoid stem cell; part of non-specific, innate immune response; nonspecifically kill certain tumor and virus infected cells; their action is up-regulated by cytokines

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40
Q

Peyer’s patches

A

large aggregates of lymphoid tissue found in the GI tract, GALT

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41
Q

lymphoid stem cells

A

T Cells, B Cells, NK cells

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42
Q

IgE

A

involved in allergy to food & respiratory allergens

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43
Q

reticuloendothelial system

A

aka. mononuclear phagocytic system. coordinates the nonspecific response to tissue injury; includes monocytes, macrophages, langerhans and glial cells

44
Q

histamine

A

released by mast cells & platelets; increases blood flow & seepage of proteins and fluid from blood

45
Q

reactive oxygen species

A

ROS; toxic for microorganisms, also damages tissue

46
Q

Interleukin-1 (IL-1)

A

triggers blood clotting; T-cell activation, decrease in BP, fever, release of prostaglandins

47
Q

prostaglandins

A

increase vascular permeability, influence platelet aggregation

48
Q

leukotrienes

A

prolong inflammatory response, vasoactive properties

49
Q

hyperemic response

A

brings neutrophils and monocytes/macrophages to injury site; supplies nutrients & O2, dilution of toxins

50
Q

vascular permeability

A

endothelial cells become “leaky” from either direct endothelial cell injury or via chemical mediators like prostaglandins

51
Q

leukocyte action/chemotaxis is controlled by

A

cellular mediators: cytokines - interleukins, interferons, colony stimulating factors (CSF); lipid mediators - platelet activating factor.

52
Q

exudate

A

fluid produced and released by injured or inflamed cells; contains proteins and immune cells

53
Q

normal WBC count

A

4300-10,000 vs 30,000 in leukocytosis

54
Q

erythrocyte sedimentation rate (ESR)

A

measures the distance RBCs have fallen after one hour; an elevated level is a laboratory marker for inflammation

55
Q

C-reactive protein (CRP)

A

a protein released asa response to inflammation; a laboratory marker of inflammation

56
Q

stages of wound healing

A

hemostasis/coagulation, inflammation, proliferation, remolding/maturation

57
Q

outcomes of inflammation

A

resolution; regeneration, repair, or transition to chronic inflammation: granuloma formation &/or nonspecific chronic inflammation

58
Q

healing by first intention

A

occurs in injury with even, closely opposed edges; clotting pathway is activated - platelet aggregation: fibrin clot forms and area is sealed

59
Q

healing by second intention

A

occurs in deep or large wounds from the bottom up;

60
Q

nutrients needed for wound healing

A

arginine, glutamine; vit. C, A, E, K; selenium, zinc

61
Q

dehiscence

A

separation of wound edges causes ineffective wound healing

62
Q

Braden Score

A

risk assessment for pressure ulcer; includes evaluation for sensory perception, moisture, activity, mobility, nutrition & friction/shear. lower score = less risk

63
Q

steroids (anti-inflammatory drugs)

A

interrupt formation of arachidonic acid; which is the precursor to many cytokines; reduces pain and swelling of inflammation

64
Q

NSAIDs

A

nonselective COX inhibitors; interrupt prostaglandin synthesis by the arachidonic pathway

65
Q

COX-2 drugs

A

inhibit enzyme pathway for generation of prostaglandins, but allow for the COX-1 protection

66
Q

COX-2

A

cyclooxygenase enzyme 2; enzyme of the arachidonic acid pathway of prostaglandin production

67
Q

T helper cell

A

secrete cytokines which help direct the immune system; express CD4 recptor

68
Q

T cytotoxic cell

A

destroy cancer cells & infected cells in an antigen-specific manner; express CD8

69
Q

T suppressor cell

A

suppress responses of T and B lymphocytes; express CD8 receptor; prevent inappropriate recognition of self-antigens

70
Q

chemical messengers which mediate the immune response

A

cytokines, ROS, histamine, prostaglandins, leukotrienes, interleukins

71
Q

artificial active immunity

A

immune response to vaccination

72
Q

natural passive immunity

A

immune response due to antibody from mother to fetus

73
Q

artificial passive

A

transferring antibodies or immune cells from one organism to another

74
Q

remission

A

A temporary or permanent decrease or subsidence of manifestations of a disease. A period during which such a decrease or subsidence occurs.

75
Q

Pathophysiology

A

The study of loss of function or the changes within an organ or organ system that occurs as a result of disease or injury. Disruption of normal physiologic processes. The sequence of events involved in tissue changes & response of the body to injury.

76
Q

Disease

A

A process that disrupts physiologic function which leads to state where homeostasis cannot be maintained.

77
Q

What are the deficiency causes of cell injury?

A

Ischemia/ Hypoxia. Nutrient deficiency. Genetic. Viral demand.

78
Q

What are the forms of cell injury caused by intoxication?

A

“Poisoning” - accumulations of toxins. Endogenous or exogenous.

79
Q

Causes of cellular injury: trauma

A

Mechanical pressure- ulcers. Physical injury. Physical agents - heat (burn), cold, radiation.

80
Q

How do cells respond to injury & disease?

A

Cellular accumulation (water, lipids, protein, pigments, minerals). Growth disturbances. Abnormal development. Inflammation & healing. Cell degeneration. Cell death.

81
Q

Intracellular accumulations in cellular injury?

A

Fluid, fat, hyaline, residual bodies -vesicles containing indigestible materials

82
Q

Examples of metaplasia

A

Squamous metaplasia. Respiratory epithelium. Cigarette smoking. Vitamin A deficiency.

83
Q

Metaplasia in Barrett’s esophagus

A

Changes to the lower esophageal epithelium. Can be caused by GERD.

84
Q

Developmental disorders

A

Maybe as a result of injury during prenatal period. Congenital vs. non congenital. ex. sickle cell, cystic fibrosis, glycogen storage disease.

85
Q

Natural or “Host” Resistance

A

Anatomical and chemical barriers - celia. Epithelial surfaces. Mucous membranes. Tears, urine, saliva. pH. Oxygen

86
Q

How are infections spread?

A

Human-to-human. Trans-placental. Blood-body fluids. Respiratory droplets. Fecal-oral. Veneraeal

87
Q

Incubation period of an infection

A

The time between entry and appearance of clinical signs.

88
Q

Prodromal period of an infection

A

Infected person may feel vague symptoms.

89
Q

Acute period of an infection

A

Disease develops fully and clinical manifestations reach their peak.

90
Q

Innate immune system

A

Nonspecific immune response. Non-adaptive. First line of defense

91
Q

Acquired immune system

A

Relies on specific immune responses selectively targeted against particular foreign material to which the body has already been exposed. Delayed reaction.

92
Q

Basic requirements of an effective immune system

A

Specificity. Diversity. Adaptivity.

93
Q

hapten

A

A non-immunogenic, low-molecular weight molecule that can be recognized by an antibody; it can initiate an immune response if it is conjugated to a “carrier” molecule.

94
Q

Primary organs of the immune system?

A

Bone marrow & thymus

95
Q

Stem cells produced in the bond marrow differentiate into what two types of cells?

A

Myeloid stem cells, of lymphoid stem cells

96
Q

Myeloid stem cells differentiate into?

A

platelets and RBCs

97
Q

Lymphoid stem cells differentiate into?

A

WBCs or leukocytes

98
Q

Functions of leukocytes?

A

Defend against invasion by pathogens. ID and destroy cancer cells; function as a clean-up crew that removes dead or injured cells.

99
Q

Antigen

A

The key to recognizing pathogens and injured cells.

100
Q

Antigen Recognitions Molecules

A

Major histocompatibility complex (MHC). Antibodies. B & T cell receptors

101
Q

Stages of the inflammatory response

A

Cellular injury, local vasodilation, phagocytes destroy injurious agents, cellular debris cleared away, protein framework for healing

102
Q

Vasomotor response in inflammation

A

Brief period of vasoconstriction. Damaged cells (mast and platelets) release histamine, serotonin, prostaglandin, luekotrienes. Vasodilation - increased blood flow.

103
Q

The hyperemic response (vasodialtion) causes?

A

The increased blood flow at the injury site brings neutrophils and monocytes to the area. It supplies needed nutrients and oxygen to site, and it dilutes toxins.

104
Q

Leukocyte action is control by

A

(chemotaxis). Cytokines, interleukins, interferons, colony stimulating factor (CSF); Lipid mediators - platelet activating factor.

105
Q

What are the local effects in inflammation

A

Increased blood flow - hyperemia –> redness and warmth. Shift of fluid into the interstitial space –> edema. Production of exudate (interstitial fluid) - has lots of RBCs.

106
Q

Factors that affect immune response

A

Nutrition. Exercise. Age, gender, hormones, stress

MD 4910 NCP I (15 decks)

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