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Pathophysiology exam 1 > Inflammation And Infectious Diseases > Flashcards

Inflammation And Infectious Diseases Flashcards

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1
Q

Inflammation

A

Body eliminated source of injury, removes damaged tissue, repairs itself
May contribute to disease

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2
Q

Cardinal signs of inflammation

A 
Redness
Swelling
Heat
Pain
Loss of function
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3
Q

Inflammatory cells

A 
Endothelium
- Line blood vessels
- Produce chemicals to maintain patently
- Produce inflammatory mediators
- Control migration of neutrophils
Leukocytes
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4
Q

Types of WBCs

A 
Neutrophils
Lymphocytes
Macrophages
Eosinophils
Basophils and mast cells
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5
Q

Neutrophils

A

Phagocytic
Secrete toxic oxygen
Arrive early
60%

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6
Q

Lymphocytes

A

B and T cells

Participate in adaptive immunity

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7
Q

Macrophages

A

Arrive within 24 hours
Clear tissue debris
Secrete cytokines, inflammatory mediators (leukotrienes, prostaglandins), and growth factors
6%

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8
Q

Eosinophils

A

Secrete mediators in response to allergies or parasites

3%

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9
Q

Basophils and mast cells

A

Secrete histamine and TNF

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10
Q

Inflammatory mediators

A

Originate from plasma or cells

  • Plasma = complement and coagulation factors
  • Cells = histamine, cytokines, etc
  • Histamine
  • Arachidonic acid metabolites
  • TNF and IL
  • Nitric oxide
  • Oxygen free-radicals
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11
Q

Histamine

A

One of first mediators released

  • Causes dilation or arteries
  • Increases vascular permeability (temporary while leukotrienes are being manufactured)
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12
Q

Arachidonic acid metabolites

A

Cytokines formed from phospholipid in cell membranes
Arachidonic acid comes from cell membranes
Precursor molecule

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13
Q

Arachidonic acid metabolite pathways

A

COX pathway - create prostaglandins -> thromboxane -> recruit platelets
Lipooxygenase pathway - creates leukotrienes

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14
Q

Prostaglandins

A

Potentiate (makes more effective) histamine and induce inflammation

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15
Q

Leukotrienes

A 
Take over for histamine
More potent
- ^ vasodilation
- ^ vascular permeability
- Attraction of inflammatory cells
- Smooth muscle contraction
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16
Q

Omega 3 fatty acids

A

Alpha linolenic acid
Eicosapentanoic acid
Docosahexainoic acid
Anti inflammatory, blood thinning, artery dilation

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17
Q

Omega 6 fatty acids

A

Linoleic acid
Gamma linolenic acid
Arachidonic acid
Pro-inflammatory, promotes blood clotting, artery constriction

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18
Q

TNF and IL

A

Cytokines produced by macrophages, lymphocytes, endothelium, and other cells
- Induce endothelial cells to express adhesion molecules (selectins)
- Release other cytokines
- Release toxic oxygen
Induce acute-phase response of systemic inflammation
- Fever
- ^ HR
- v hunger
- ^ neutrophils
- ^ corticosteroids

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19
Q

Nitric oxide

A

Smooth muscle relaxation

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20
Q

Oxygen free-radicals

A

Increase expression of cytokines

Very reactive - can cause cellular damage

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21
Q

Acute inflammation

A

Immediate and localized
Components:
- Vascular changes
- Cellular changes

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22
Q

Vascular changes of acute inflammation

A

Transient vasoconstriction, then vasodilation
- Induced by histamine and nitric oxide
Increased vascular permeability follows
- Chemical mediators bind to endothelial cells, cause contraction, create gaps between endothelial cells
- Movement of protein rich fluid into extravascular space
- Increased osmotic pressure of extravascular space/interstitial tissue pulls fluid

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23
Q

Types of exudates

A

Serous - watery, yellowish fluids
Serosanguinous - some RBCs
Hemorrhagic (sanguinous) - leakage of RBCs
Fibrinous - contains fibrinogen (forms thick mesh)
Purulent - contains pus

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24
Q

Cellular changes

A

Changes in endothelium and movement of leukocytes into area of injury
Recruitment involves chemical mediators (mast cells)

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25
Phases of cellular changes
``` Marination Adhesion Transmigration Chemotaxi Leukocytes activation Phagocytosis ```
26
Margination
Accumulation of leukocytes at site of injury
27
Adhesion
Cytokines stimulates endothelial cells to express adhesion molecules (selectins) Bind to leukocyte (tethering) Roll along endothelial lining Come to rest and adhere to intracellular adhesion molecules - “firm adhesion”
28
Transmigration
Adhesion causes endothelial cells to separate | Leukocytes move between endothelial cells into tissue spaces
29
Chemotaxis
Movement of leukocytes to site of injury directed by chemokines
30
Leukocyte activation
Chemicals at site of injury
31
Phagocytosis
Recognition and adherence - Depends on type of cell - recognized by receptor or opsonization Engulfment - Binding triggers endocytosis Intracellular killing - Phagosome merges with lysosome to destroy pathogen
32
Chronic inflammation
Infiltration of macrophages and lymphocytes rather than neutrophils Fibroblasts instead of protein rich exudates Often caused by persistent infection or irritants that don’t spread rapidly More B and T cells than macrophages
33
Non-specific chronic inflammation
Diffuse accumulation of these cells
34
Granulomatous chronic inflammation
Constantly release chemical to try and eliminate pathogens | Associated with foreign bodies and some microorganisms
35
Systemic inflammation
Systemic response from release of inflammatory mediators into circulation
36
Acute phase response of systemic inflammation
Begins hours-days Triggered by IL and TNF Affect thermoregulatory system to create fever Stimulate bone marrow to create neutrophils Lack of appetite, sleepiness, aches by CNS response Can lead to SIRS
37
Lymphadenitis
Inflammatory mediators produced by inflammation cause reaction when drained into lymph nodes Painful, palpable nodes
38
Tissue repair processes
Tissue regeneration | Fibrous tissue repair
39
Tissue regeneration
``` Replacement of damage tissue with the same cell type: Parenchyma cells - functional - Recreation won't leave a scar Stromal cells - supportive - Will leave a scar ```
40
Capacity for regeneration
Varies by cell type Labile - constantly regenerate (skin) Stable - stop dividing, but can regenerate if signaled to do so (liver) Permanent - do not regenerate (heart)
41
Fibrous tissue repair
Replacement of damaged tissue with connective tissue Occurs with severe or repeated injury to parenchyma and stromal tissue - Generation of granulation tissue - Moist, red connective tissue - Angiogenesis from existing vessels - Foundation of new tissue Fibrogenesis - Influx of fibroblasts laying down loose ECM made of fibronectin, hyaluronic acid, and proteoglycans - Proteoglycans (hydrophilic) are responsible for swelling Scar formation - Fibroblasts increase synthesis of collagen - Vessels in granulation tissue degenerate - Mature scar develops
42
Wound healing
``` Primary intention - Sutured wound - Faster Secondary intention - Pressure ulcer, burn - Slower - Granulation tissue develops, heals on outside, works towards middle - Prone to infection Approximating wound - taking edges and stitching together - Heals bottom-up ```
43
Phases of wound healing
Inflammation - Preps wound for healing - Vasoconstriction followed by vasodilation - Influx of neutrophils and macrophages Proliferative - 2-3 days of injury - Fibroblasts create granulation tissue, collagen, ECM - Release growth factor that stimulate angiogenesis - Epithelial cells are produced at wound edges Remodeling - 3 weeks after injury - Structure of scar changes - Vascularity decreases - Generation of collagen by fibroblasts - Lysis of collagen by enzymes - Wound contraction results in shrinkage of scar
44
Mechanisms of infectious diseases
``` Prions - Protein particles - mutation of normal host protein - Cause non-inflammatory degeneration of neurons - Creutzfeldt-Jakob and Mad Cow disease Viruses - Made of protein coat and nucleic acid code - Can't replicate outside of living cell - May insert itself into genome of host cell Bacteria - Unicellular organisms - No organized nucleus - High adaptable Fungi - Organized nucleus - Yeasts, molds Parasites - Derive benefit from host - Unicellular or multicellular - Protozoa (giardia lamblia) - Helminths (ascaris) - Arthropods (ticks, fleas) ```
45
HIV
Malignancy Body wasting CNS degeneration
46
Reproduction of HIV
Retrovirus - has RNA and creates DNA - Binds with host cell and inserts itself into DNA - Reverse transcriptase makes DNA from RNA to make a double strand of DNA - Viral DNA incorporates itself into CD4 cell - DNA is read and creates nucleic acids and protein coats - Creates virus and destroys CD4 cell
47
Transmission of HIV
Blood to blood contact or perinatally | Infected blood, semen, or vaginal secretions come into contact with mucous membranes or bloodstream of another
48
Window period
When an infected person can pass the virus in the absence of symptoms
49
Seroconversion
Positive presence of HIV antibodies in blood - Characterized by CD4 - Count <200 is AIDs
50
Rickettsiaceae and Chlamydiaceae
Combine characteristics of viruses and bacteria - Cannot replicate outside of host cell - Produce rigid cell wall, reproduce asexually, contain DNA and RNA Depend on host cell for nutrients Rickettsiaceae from arthropod bite and Chlamydiaceae transmitted directly
51
Stages of infection
Incubation - pathogen replicating slowly, no symptoms in host Prodromal - initial appearance of symptoms Acute - max. replication of pathogen and symptoms, inflammatory/tissue damage occurring Convalescent - containment, tissue repair, resolution of symptoms Resolution - total elimination
52
Host defenses
Secretions in mucosal membranes Lysozyme in tears dissolve peptidoglycan in bacterial wall Skin - Low pH and presence of fatty acids - Maceration - when skin shrivels on itself GU tract - Sterile Respiratory tract - Mucociliary blanket lining nose and upper resp. tract trap microbes - Goblet cells secrete mucous - Cilia in upper airway move bacteria to back of throat to swallow/expel - Alveolar macrophages destroy small organisms GI tract - Gastric acid - Viscous mucous layer coats gut - Pancreatic enzymes and bile - IgA secreted by mucous membranes
53
Factors enhancing virulence
Toxins Adhesion factors Evasive factors Invasion factors
54
Exotoxins
Proteins released by bacteria during growth | - Enzymatically alter components of host cell -> dysfunction or death
55
Endotoxins
Lipid and polysaccharide in cell wall of G- bacteria
56
Adhesion factors
Special filaments that enable pathogens to attach to host
57
Evasive factors
Means by which pathogens avoid immune system of host | - Capsules, chemical release, ability to survive within leukocytes
58
Invasive factors
How pathogens invade host
59
Antimicrobial resistance
Associated with extended hospitalization, significant morbidity, increased mortality
60
Acquisition of resistance
Spontaneous mutation - Random alteration in DNA Conjugation - Transfer of genetic material from one organism to another
61
How do bacteria resist antibiotics?
``` Reduced concentration of drug at site of action - Site is intracellular - Cease active uptake - Increase active export Alteration of drug target molecule - Cell receptors - Ribosomes Production of antagonist Inactivation of drug - Produce drug-metabolizing enzymes ```
62
Immunotherapy
Supplementing or stimulating immune system of host to limit spread of pathogen - IV immune globulin (antibody given in IV to fight infection - not created by body) - Cytokines - Immunization
63
Active immunity
Developed by vaccination or having the disease Body exposed to antigen and develops its own immunity Immune system responds by creating antibodies
64
Passive immunity
Immunity from another Fetus protected by IgG of mother Hyperimmune serum
65
Blood vessel layers
``` Tunia intima - Remain smooth - Release cytokines and other inflammation factors - Maintains potency (openness) - Control migration of neutrophils Tunia media Tunia externa ```
66
SIRS
Systemic inflammatory response syndrome - Vasodilation - BP plummets, difficult to get blood to the brain - ^ HR as compensation - Body constricts vessels to less important areas

Pathophysiology exam 1 (3 decks)

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