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pathophysiology exam 1 > Inflammation And Infectious Diseases > Flashcards

Inflammation And Infectious Diseases Flashcards

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
Q

Phases of cellular changes

A 
Marination
Adhesion
Transmigration
Chemotaxi
Leukocytes activation
Phagocytosis
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26
Q

Margination

A

Accumulation of leukocytes at site of injury

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27
Q

Adhesion

A

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
Q

Transmigration

A

Adhesion causes endothelial cells to separate

Leukocytes move between endothelial cells into tissue spaces

29
Q

Chemotaxis

A

Movement of leukocytes to site of injury directed by chemokines

30
Q

Leukocyte activation

A

Chemicals at site of injury

31
Q

Phagocytosis

A

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
Q

Chronic inflammation

A

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
Q

Non-specific chronic inflammation

A

Diffuse accumulation of these cells

34
Q

Granulomatous chronic inflammation

A

Constantly release chemical to try and eliminate pathogens

Associated with foreign bodies and some microorganisms

35
Q

Systemic inflammation

A

Systemic response from release of inflammatory mediators into circulation

36
Q

Acute phase response of systemic inflammation

A

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
Q

Lymphadenitis

A

Inflammatory mediators produced by inflammation cause reaction when drained into lymph nodes
Painful, palpable nodes

38
Q

Tissue repair processes

A

Tissue regeneration

Fibrous tissue repair

39
Q

Tissue regeneration

A 
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
Q

Capacity for regeneration

A

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
Q

Fibrous tissue repair

A

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
Q

Wound healing

A 
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
Q

Phases of wound healing

A

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
Q

Mechanisms of infectious diseases

A 
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
Q

HIV

A

Malignancy
Body wasting
CNS degeneration

46
Q

Reproduction of HIV

A

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
Q

Transmission of HIV

A

Blood to blood contact or perinatally

Infected blood, semen, or vaginal secretions come into contact with mucous membranes or bloodstream of another

48
Q

Window period

A

When an infected person can pass the virus in the absence of symptoms

49
Q

Seroconversion

A

Positive presence of HIV antibodies in blood

  • Characterized by CD4
    • Count <200 is AIDs
50
Q

Rickettsiaceae and Chlamydiaceae

A

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
Q

Stages of infection

A

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
Q

Host defenses

A

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
Q

Factors enhancing virulence

A

Toxins
Adhesion factors
Evasive factors
Invasion factors

54
Q

Exotoxins

A

Proteins released by bacteria during growth

- Enzymatically alter components of host cell -> dysfunction or death

55
Q

Endotoxins

A

Lipid and polysaccharide in cell wall of G- bacteria

56
Q

Adhesion factors

A

Special filaments that enable pathogens to attach to host

57
Q

Evasive factors

A

Means by which pathogens avoid immune system of host

- Capsules, chemical release, ability to survive within leukocytes

58
Q

Invasive factors

A

How pathogens invade host

59
Q

Antimicrobial resistance

A

Associated with extended hospitalization, significant morbidity, increased mortality

60
Q

Acquisition of resistance

A

Spontaneous mutation
- Random alteration in DNA
Conjugation
- Transfer of genetic material from one organism to another

61
Q

How do bacteria resist antibiotics?

A 
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
Q

Immunotherapy

A

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
Q

Active immunity

A

Developed by vaccination or having the disease
Body exposed to antigen and develops its own immunity
Immune system responds by creating antibodies

64
Q

Passive immunity

A

Immunity from another
Fetus protected by IgG of mother
Hyperimmune serum

65
Q

Blood vessel layers

A 
Tunia intima
- Remain smooth
- Release cytokines and other inflammation factors
- Maintains potency (openness)
- Control migration of neutrophils
Tunia media
Tunia externa
66
Q

SIRS

A

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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