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Pathophysiology > Innate Immunity, Inflammation, and Stress > Flashcards

Innate Immunity, Inflammation, and Stress Flashcards

1
Q

What are the three levels of immunity?

A

(1) first line of defense = innate (natural or native) immunity
making presence known

(2) second line of defense = inflammation
full force

(3) third line of defense = adaptive (acquired or specific) immunity
specific approach

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2
Q

Describe aspects of innate immunity

A
  • natural physical barriers, mechanical, biochemical barriers
  • inflammation
  • in place at birth
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3
Q

Examples of physical barriers

A
  • skin
  • lining of gastrointestinal, genitourinary, and respiratory tracts
  • mucous and cilia trap organisms and expel them through coughing, sneezing, urination, vomiting, and defecation
  • low temp and low pH inhibit microorganism growth
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4
Q

Examples of cell-derived chemical barriers

A
  • mucus, sweat, saliva, tears, earwax
  • lysozyme attacks cell walls of gram-positive bacteria
  • sebaceous glands secrete fatty acids and lactic acid that kill bacteria and fungi and create acidic pH
  • antimicrobial peptides kill or inhibit growth of bacteria, fungi, and viruses (collectins and defensins)
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5
Q

Describe the normal microbiome

A
  • each body surface is colonized by nonpathogenic microorganisms unique to the particular location and individual
  • commensal or mutualistic relationship
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6
Q

Functions of the normal microbiome

A
  • produces enzymes for digestions
  • synthesizes metabolites
  • releases antibacterial substances
  • competes with pathogens for nutrients
  • fosters adaptive immunity
  • helps with communication between brain and GI tract
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7
Q

What are the categories of innate immunity white blood cells?

A
  • endothelial cells (physical barrier)
  • platelets
  • granulocytes (release chemicals and phagocytize)
  • agranulocytes (phagocytize)
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8
Q

Describe function and types of granulocytes

A

(1) neutrophils → first responder, phagocytosis

(2) eosinophils → release chemicals, allergy response, mildly phagocytize (parasites)

(3) basophils → release chemicals, allergy response

(4) mast cells → sentinel, release chemicals

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9
Q

Describe function and types of agranulocytes

A

Monocytes (macrophages) → inflammatory response, phagocytosis

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10
Q

Function of inflammation

A
  • programmed response to damage/injury in the body/cell
  • all or nothing first response → occurs in any vascularized tissue; rapid; nonspecific
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11
Q

Benefits of inflammation

A
  • generates new tissue
  • limits and controls inflammatory process → clotting, plasma enzymes and cells will localize response
  • prevent and limits infection/further damage → influx of plasma dilutes toxins, activates plasma protein systems, brings cells that will destroy infectious agents
  • prepares injury for healing and repair → dead cells and bacteria products removed
  • facilitates development of adaptive immune response (more specific)
  • nonspecific
  • prevents you from dying!
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12
Q

Steps of inflammation process (vascular response)

A

(1) vasodilation (increased size of blood vessels) → slower blood velocity; increased blood flow to injured site; plasma-derived mediators involved

(2) increased vascular permeability (platelets) → blood vessels become more porous from endothelial cell contractions; fluid/chemicals leak out (exudation and edema); slower blood flow and increased blood viscosity; increased concentration of RBCs at injury site cause redness (erythema) and warmth

(3) hemostasis: coagualtion/clotting

(4) white blood cell adherence to vessel walls (platelets) & migration through the capillary bed (chemotaxis) → “leukocyte rolling”

(5) leukocyte activation and phagocytosis → secretion/degranulation of compounds

  • leukocytes (neutrophils), plasma proteins, other biochemical mediators delivers to injury site → can activate pain fibers → injury, pain, and swelling contribute to loss of function
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13
Q

Describe phagocytosis

A
  • process by which a cell ingests and disposes of foreign material (neutrophils and macrophages)
  • cells must leave circulation and migrate to site of inflammation
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14
Q

Steps of phagocytosis

A

(1) recognition and adherence to target

(2) engulfment (ingestion or endocytosis)

(3) formation of phagosome (cell membrane covered in foreign object)

(4) fusion of phagosome with lysosomal granules

(5) destruction of target

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15
Q

List phagocytes

A

(1) neutrophils

(2) monocytes and macrophages

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16
Q

Describe neutrophil role in phagocytosis

A
  • first responder
  • short life span
  • becomes component of pus (what it digested and spit out) → keeps area clean
  • removes debris and dead cells
  • destroys bacteria
  • chemotaxic for monocytes
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17
Q

Describe monocyte and macrophage role in phagocytosis

A
  • monocytes (produced in bone marrow) circulate in blood stream
  • migrate to inflammatory site and develop into macrophages after 24 hours (replacing neutrophils)
  • long term action → divide and survive longer
  • orchestrate wound healing by phagocytizing debris, promoting angiogenesis, releasing cytokines and growth factors, activating fibroblasts, promoting synthesis of collagen
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18
Q

Describe eosinophil role in phagocytosis

A
  • mildly phagocytic
  • primary defense against parasites
  • help regulate vascular mediators from mast cells
  • limit and control inflammation
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19
Q

Describe dendritic cell role in phagocytosis

A
  • link between innate and adaptive immunity through interaction with T lymphocytes
  • phagocytic to find out what invader is made of
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20
Q

Which leukocytes participate in the acute inflammatory response?
A - Eosinophils
B - Monocytes
C - Neutrophils
D - All of the above
E - A and C

A

D - all of the above

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21
Q

What is the correct timeline of inflammatory events?
- Immune Cell infiltration
- Vascular response (hemostasis; vasodilation, increased permeability)
- Immune Cell Activation (degranulation & phagocytosis)

A

(1) Vascular response (hemostasis; vasodilation, increased permeability)

(2) Immune Cell infiltration

(3) Immune Cell Activation (degranulation & phagocytosis)

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22
Q

Difference between plasma-derived and cell-derived inflammatory mediators

A

plasma-derived:
- produced in liver
- released into blood stream (float around plasma)
- activated at site of injury (can start inflammatory process)

cell-derived:
- from bone marrow
- in the blood stream (local)
- released at site of injury by cells floating around intravascular compartment to start inflammation

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23
Q

Types of plasma-derived inflammatory mediators

A

(1) complement system

(2) coagulation (clotting) system

(3) kallikrein-kinnogen system (kinin)

  • always around and inactive
  • all contain inactive enzymes (proenzymes) that must be converted to be active → once active, can initiate cascade
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24
Q

Role of plasma-derived inflammatory mediators in inflammation

A

(1) vasodilation/vascular permeability

(2) leukocyte activation, adhesion, and chemotaxis

(3) augmenting phagocytosis

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25
Q

Describe complement system

A
  • activation of C3 and C5 → opsonins, chemotactic factors, anaphylatoxins, cell lysis
  • large number of proteins (10% of total serum proteins)
  • produces biologically active fragments that recruit phagocytes, activate mast cells, and destroy pathogens
  • inactive → active
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26
Q

Pathways of complement system activation

A

(1) classical (antibody/antigen)

(2) lectin (receptor - PAMP/DAMP)

(3) alternative (spontaneous, pathogenic surfaces)

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27
Q

Describe classical pathway of complement system activation

A
  • primarily activated by antibodies (proteins of acquired immune system)
  • antibodies activate C1 → activation of other complement components → activation of C3 and C5 → activate molecules to kill bacteria and activate inflammation
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28
Q

Describe alternative pathway of complement system activation

A
  • activated by substances found on surface of pathogen
  • uses unique proteins to form a complex that activates C3 → C5 activation → converges with classical pathway
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29
Q

Describe lectin pathway of complement system activation

A
  • activated by plasma proteins
  • binds to bacteria → activate C3 and C5
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30
Q

Functions of C3 and C5 activation

A

(1) opsonins → mark for phagocytosis

(2) anaphylatoxins → hemostasis: smooth muscle contractions and vasodilation; histamine released from mast cells; enhanced vascular permeability

(3) leukocyte chemotaxis

(4) cell lysis

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31
Q

Describe clotting system

A

fibrinogen (activated by enzymes from injury) → fibrin (protein that sticks to itself) → clot

  • clots plug damaged vessels to stop bleeding, trap microorganisms to prevent spread/infection
  • activated by substances released during cell injury and infection and by bacterial products → increase inflammatory response and enhance chemotaxis and vascular permeability
  • provides framework for repair and healing → (1) tissue factor (extrinsic - outside damage); (2) contact activation (intrinsic - stressors on endothelial cell that causes damage)
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32
Q

Describe kallikrein-kininogen system (kinin)

A
  • works closely with clotting system
  • can be initiated through activation of Hageman factor (factor XII)
  • produces bradykinin → molecule responsible for inflammation
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33
Q

Role of primary kininis (bradykinin)

A
  • dilation of blood vessels
  • acts with prostaglandins to induce pain
  • smooth muscle cell contraction (bleeding)
  • increased vascular permeability
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34
Q

Describe cellular-derived inflammatory mediators

A
  • released from cells
  • respond to molecules at site of damage and are recruited there
  • cell surface receptors bind to molecules and activate intracellular signaling pathways and the cell
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35
Q

Functions of cellular-derived inflammatory mediators

A

inflammation:
- confine extent of damage

  • kill microorganisms
  • remove cellular debris
  • activate healing/tissue regeneration
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36
Q

Define pattern recognition receptors (PRRs)

A
  • monitor for cellular damage and microorganisms
  • recognize: (1) PAMPS → pathogen-associated molecular patterns; (2) DAMPS → damage-associated molecular patterns
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37
Q

Types of PRRs

A
  • toll-like receptors
  • c-type lectin receptors
  • nucelotide-binding-like receptors
  • NOD-like receptors
  • complement receptors
  • scavenger receptors
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38
Q

Define endothelium

A
  • cells of the vessel wall that adhere to an underlying matrix of connective tissue
  • regulates circulating levels of inflammatory mediators and prevents spontaneous activation of clotting system
  • have receptors that lead to activation of cell-derived mediators
  • will release things if something goes wrong! ex: nitric oxide (NO) and prostacyclin (PGl2) → from arachidonic acid (inhibited by NSAIDs which decrease vasodilation)
39
Q

Role of endothelium in inflammation

A

when endothelial cells are damaged it exposes underlying matrix which stimulates clotting and inflammation

40
Q

Describe platelets

A
  • cytoplasmic fragments from megakaryocytes (large bone marrow cell)
  • circulate in bloodstream
  • activated by products of tissue destruction
41
Q

How are platelets activated?

A

interact with components of coagulation cascade and degranulate/release chemical mediator serotonin (vasodilator) and growth factors that promote healing

42
Q

Describe mast cells

A
  • most important cellular activator in inflammatory response
  • filled with granules
  • in loose connective tissues close to blood vessels near body’s outer surfaces
  • sentinel
43
Q

Role of mast cells in inflammation

A
  • degranulate/release contents; quick response
  • ex: histamine (vasoactive amine) → causes temporary, rapid constriction of smooth muscle and dilation of postcapillary venules → increased blood flow → increased vascular permeability → increased adherence of leukocytes to endothelium

begin new synthesis of:
- leukotrienes: histamine-like but slower with more prolonged response

  • prostaglandins: increase vascular permeability, stimulate chemotaxis, stimulate pain nerve endings
  • platelet-activating factor (PAF): vascular permeability, leukocyte adhesion to endothelial cells, platelet aggregation
44
Q

Describe basophils

A
  • found in the blood
  • function similarly to mast cells
  • release histamine/cytokines
45
Q

Define cytokines

A
  • molecules that affect other cells
  • all over inflammatory process
  • can be pro-inflammatory or anti-inflammatory (alter behavior of cells)
  • diffuse over short distances or intravascular travel; bind to target cells; affect cellular function (activation or production of other cytokines)
  • interleukins or interferons
46
Q

Define chemokines

A
  • attract leukocytes (chemotaxis)
  • synthesized by many cells (macrophages, fibroblasts, endothelial cells)
47
Q

Define interleukins (ILs)

A
  • produced by macrophages and lymphocytes in response to stimulation by pathogens, products of cellular damage, or other cytokines
48
Q

Effects of interleukins

A
  • alteration of adhesion molecule expression
  • attraction of leukocytes (chemotaxis)
  • induction, proliferation, and maturation of leukocytes
  • enhancement or suppression of inflammation and adaptive immune response
49
Q

Describe IL-1

A
  • produced mainly by macrophages
  • activates monocytes, other macrophages, and lymphocytes (acts as growth factor)
  • stimulates chemotaxis and proliferation of immune cells
  • endogenous pyrogen (compound that creates fever → IL-6 recognized by hypothalamus which regulates temperature)
50
Q

Describe IL-6

A
  • produced by macrophages, lymphocytes, fibroblasts, and other cells (muscle)
  • induces hepatocytes to produce acute phase reactants (needed for inflammation)
  • stimulates growth and differentiation of blood cells and fibroblasts (needed for wound healing)
51
Q

Describe tumor necrosis factor-alpha (TNF-α)

A
  • secreted by macrophages and other cells (mast cells) in response to stimulation by toll-like receptors
  • highly inflammatory → induces fever (pyrogen), increased synthesis of other inflammatory mediators, causes muscle wasting
  • high levels are lethal and can lead to sepsis/septic shock (decreased blood pressure
52
Q

Define sickness behavior

A
  • IL-6, IL-10, TNF-α
  • lethargy, depression, anxiety, malaise, loss of appetite, sleepiness, hyperalgesia, reduction in grooming, failure to concentrate
  • tells our brain that we’re sick
53
Q

Define interferons (IFNs)

A
  • protect against viral infections
  • signal nearby cells to produce antiviral proteins
54
Q

Describe interleukin-10 (IL-10)

A
  • anti-inflammatory interleukin
  • suppresses activation and proliferation of other lymphocytes
  • limits production and pro-inflammatory cytokines
  • produced by lymphocytes
55
Q

Describe transforming growth factor-beta (TGF-β)

A
  • anti-inflammatory interleukin
  • suppresses activity of lymphocytes
  • downregulates production of pro-inflammatory cytokines
56
Q

Which inflammatory mediators come from the liver?
A - Mast Cells
B - Leukocytes
C - Complement
D - B Cell

A

C - Complement (plasma-derived)

57
Q

What is the role of plasma-derived mediators?
A - Innate Immunity B - Adaptive Immunity
C - Inflammation
D - Wound healing

A

C - Inflammation

58
Q

Name two ways complement protein participate in innate immunity/inflammation?

A

(1) opsonisation
(2) cell lysis
(3) chemotaxis
(4) anaphalytoxin

59
Q

List the three cytokines responsible for sickness behavior?

A

(1) IL-6

(2) IL-1

(3) TNF-α

60
Q

Define exudate

A

a mass of cells and fluid that has seeped out of blood vessels or an organ (especially in inflammation)

61
Q

Define serous exudate

A
  • early or mild inflammation
  • very few plasma proteins or leukocytes
  • watery
62
Q

Define serosanguinous exudate

A
  • some blood with serous
  • pinkish
63
Q

Define fibrinous exudate

A
  • severe or advanced inflammation
  • thick and clotted (over-activation of clotting system)
  • fibrin/fibrinogen proteins in clotting
64
Q

Define purulent exudate

A
  • pus
  • large number of leukocytes (infiltration and activation of immune cells)
  • cellular debris
  • clotting factors
  • characteristic of walled off lesions (Cysts or abscesses)
65
Q

Define sanguinous or hemorrhagic exudate

A
  • very bloody
  • lots of capillaries damaged
66
Q

Define membranous or pseudomembranous exudate

A
  • on mucous membrane
  • with necrotic tissue
67
Q

Define ulceration

A

site of inflammation where an epithelial surface is necrotic and eroded

68
Q

Characteristics of systemic manifestations of acute inflammation

A
  • fever/lethargy: from cytokines that act as endogenous pyrogen
  • leukocytosis: increase in number of circulating white blood cells (greater than 10,000/ml3)
  • plasma protein synthesis: acute-phase reactants
    → most produced by liver
    → pro- or anti- inflammatory
    → C-reactive protein (CRP), complement components, fibrinogen
    → will increase erythrocyte sedimentation rate (ESR); increased ESR = liver increased production of fibrinogen
69
Q

Describe chronic inflammation

A
  • lasts longer than 2 weeks
  • unsuccessful acute inflammatory response
  • suppuration (discharge), pus formation, incomplete wound healing
  • dense infiltration of lymphocytes and macrophages
  • granuloma can form (walling off and isolation of infected/inflamed area)
  • ex: TB
70
Q

General phases of wound repair

A

(1) hemostasis (stop clotting & inflammation), angiogenesis, ingrowth of granulation (new) tissue

(2) emigration of fibroblasts and deposition of extracellular matrix

(3) maturation and reorganization of the fibrous tissue (remodeling)

  • within 24 hrs of injury
  • migration of fibroblasts & induction of fibroblast + epithelial cell proliferation
71
Q

Differences between primary and secondary intention in wound healing

A

primary = most wounds
- minimal tissue loss
- healing more rapid

secondary = usually stitches
- open wound (pressure ulcer)
- loss of tissue
- slower healing and repair time
- greater scarring
- greater chances of infection

repaired tissue = 80% of tensile strength

cells replaced are not cells lost (decrease in function)
- except epithelial, bone marrow, and liver cells

72
Q

Phase 1 of cutaneous wound healing

A

(1) Hemostasis Phase (immediate)
- coagulation/clot formation
- fibrin mesh of blood clots for future cells
- platelets degranulate (capillary permeability & release growth factor)
- bradykinin

73
Q

Phase 2 of cutaneous wound healing

A

(2) Inflammatory Phase (1-2 days)
- infiltration + activation of wound healing cells (ex: neutrophils, macrophages, and lymphocytes)
- redness
- pain
- releasing cellular-derived mediators
- damaged cells + pathogens removed

74
Q

Phase 3 of cutaneous wound healing

A

(3) Proliferative Phase (3-14 days)
- macrophages clear debris + secrete chemicals that stimulate fibroblasts (lay down connective tissue + collage) to synthesize and secret procollagen, stimulate angiogenesis, and promote wound healing

  • granulation tissue grows into wound (new capillaries & very red appearance)
  • epithelialization (scab formation): epithelial cells migrate under clot or scab and form new skin
  • fibroblasts: secrete collagen (forms crosslinks)
  • myofibroblasts: responsible for would contraction (brings tissue together to close wound)
75
Q

Phase 4 of cutaneous wound healing

A

(4) Remodeling Phase (several weeks-2 years)
- continued cellular differentiation
- scar formation
- scar remodeling
- wounds that heal with too much scar tissue → keloids (cell division doesn’t stop); scar is avascular

76
Q

Fibroblasts, endothelial cells, and epithelial cells divide during which
phase of wound healing?
A - Inflammatory phase
B - Proliferative phase
C - Remodeling

A

B - Proliferative phase

77
Q

Examples of dysfunctions in wound healing

A
  • ischemia: impairs collagen synthesis and strength of regenerating tissue (susceptible to infection and delay in healing)
  • excessive bleeding: large clots = more space for granulation tissue to fill → accumulated blood = bacterial growth
  • excessive fibrin: forms barrier/excessive clotting
  • diabetes: small vessels → impaired microcirculation; hyperglycemia impairs macrophages and feeds bacteria
  • wound infection
  • nutrition: protein, vitamins A + C, zinc, iron, manganese, copper
  • medications
  • elderly
  • dehiscence
  • contracture
78
Q

Define dehiscence

A

wound separation (during first proliferation phase)
- 5-12 days after surgery highest risk
- increased risk with obesity (not as well vascularized)
- increased risk with abdominal wounds

evisceration = internal structures become externalized after dehiscence

79
Q

Define contracture

A

excessive contraction of wound
- problematic with skin over joints and healing in GI tract
- occurs more with loose skin (ex: neck, elbow)

80
Q

List the phases in wound healing in the correct order
- Ingrowth of granulation (new) tissue
- Hemostasis & angiogenesis
- Maturation and reorganization of the fibrous tissue
(remodeling)
- Emigration of fibroblasts and deposition of the extracellular
matrix

A

(1) Hemostasis & angiogenesis

(2) Emigration of fibroblasts and deposition of the extracellular
matrix

(3) Ingrowth of granulation (new) tissue

(4) Maturation and reorganization of the fibrous tissue
(remodeling)

81
Q

Define stress

A
  • perceived or anticipated threat that disrupts a person’s well-being or homeostasis
  • demands can be physical (cold temperatures, moving heavy equipment) or psychological (meeting deadlines, balancing assignments)
82
Q

Physiologic stress involves:

A
  • enlargement of adrenal gland
  • decreased leukocyte numbers/function
  • increased/decreased inflammatory response
  • increased coagulability
  • development of bleeding ulcers in the stomach
83
Q

Define general adaptation syndrome

A

physiologic stress impairs the ability to resist future stressors → stress response system defends then fatigues

84
Q

Stages of general adaptation syndrome

A

(1) alarm stage
- secretion of hormones and catecholamines to prepare for emergency reaction
- arousal of body defenses

(2) resistance/adaptation stage
- brain continuously monitors for future events and anticipates what is required from neuroendocrine and autonomic system
- mobilization of body’s resources to handle sustained challenges
- allostasis: stability through change

(3) exhaustion stage (allostatic overload)
- occurs when stress continues and adaption is not successful
- leads to stress-related disorders
- impacts immune system and inflammation

85
Q

Describe HPA stress

A

hypothalamus-pituitary gland-adrenal axis
- hypothalamus secretes CRH → pituitary releases ACTH → adrenals secret cortisol

  • regulates arousal, cognition, mood, sleep, metabolism, cardiovascular tone, growth, and reproduction
  • stimulates gluconeogenesis
  • increases protein metabolism
  • powerful anti-inflammatory and immunosuppressive agent
86
Q

Chronic, abnormal elevations of cortisol may cause:

A

chronic, abnormal elevations of cortisol may cause:
- obesity, sleep deprivation, lipid abnormalities, hypertension, diabetes, atherosclerosis, and loss of bone density

  • cognitive impairments, emotional disorders
  • gastric ulcers
  • increased baseline inflammation
  • increased cortisol = decreased immune response
87
Q

Describe SNS stress

A

sympathetic nervous system
- activation of SNS induces rapid release of catecholamines → norepinephrine, epinephrine

  • regulate cardiovascular, pulmonary, hepatic, skeletal muscle, and immune systems
  • increases heart rate and blood pressure
  • increases pro-inflammatory cytokine production
88
Q

Chronic stress-induced release of norepinephrine may cause:

A
  • plaque formation in blood vessels (clots)
  • thrombi (sticky)
  • emboli (floating)
  • myocardial infarction (heart attack)
  • stroke
89
Q

Describe immune stress

A
  • immune cells have receptors for products of stress response
  • decreases immunity
90
Q

Define primary deficiencies in immunity

A
  • congenital/genetic
  • principal component of immune system that is defective
91
Q

Three classifications of primary deficiencies in immunity

A

(1) complement
- C3 deficiency (doesn’t make complement)
- most severe defect due to central role in compliment cascade
- results in recurrent life-threatening infections

(2) phagocyte
- chronic granulomatous disease (CGD)
- defect in myeloperoxidase-hydrogen peroxide system
- causes deficient production of products needed for phagocytic killing
- results in recurrent pneumonia; tumorlike granulomata in lungs, skin, bones, and other infections

(3) innate
- chronic mucocutaneous candidiasis
- severe recurrent candida infections due to defective immune response to C. albicans

92
Q

Define acquired/secondary deficiencies in immunity

A
  • more common
  • caused by another illness
  • pregnancy, infancy, aging, emotional trauma, eating disorders, dietary insufficiencies (malnutrition), malignancies, burns, medical treatments, diabetes, alcoholic cirrhosis, immunosuppressant drugs, AIDs
93
Q

Categories of adaptive white blood cells

A

(1) T lymphocytes

(2) B lymphocytes (plasma cells)

94
Q

Symptoms of acute inflammation

A
  • redness (erythema)
  • heat (blood flow)
  • swelling (edema)
  • pain (bradykinin)
  • loss of function
  • less than 2 weeks

Pathophysiology (6 decks)

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