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General Pathology -- Roecker > Gen Pathology Exam 1 Section 2: Inflammation and Repair > Flashcards

Gen Pathology Exam 1 Section 2: Inflammation and Repair Flashcards

1
Q

Neutrophils

A

granulocytes; most abundant (~70% all circulating WBC’s); perform phagocytosis at site of ACUTE inflammation

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2
Q

Basophils

A

granulocytes; ~1% all WBC’s; involved in allergic reactions (asthma, anaphylaxis, atopic dermitis, and allergic rhinitis)

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3
Q

Eosinophils

A

granulocytes; ~3% all WBC’s; commonly involved with parasitic infections and allergic reactions

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4
Q

Monocytes/Macrophages

A

agranulocytes; (~10% all WBC’s); Monocytes differentiate into Macrophages when “activated” at site of CHRONIC inflammation
Macrophages–> preform phagocytosis

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5
Q

Lymphocytes

A

agranulocytes; ~25% of all WBC’s; Numerous categories (Tcells, Bcells, NK cells); at CHRONIC inflammation sites

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6
Q

T-cells

A

NOT a single type of cell; represent a group of similar but different types of cells ( cytotoxic T cells, T helper cells, and B cells)

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7
Q

B cells

A

transition into plasma cells

Plasma Cells = the primary cell involved with antibody production (adaptive immunity)

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8
Q

What cells function as sentinel cells for infection or injured tissues?

A

macrophages
dendritic cells
mast cells
—they secrete cytokines = pro-inflammatory

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9
Q

Acute Inflammation

A

initial response to injury or infection; develops with in minutes of initial stimulus; lasts hrs to days
Main cell = neutrophils
Produces–> fever, rigors, body aches, or headaches
- Unlikely to result in fibrosis

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10
Q

Cardinal Signs of Inflammation

A
  1. redness
  2. heat
  3. swelling
  4. pain
  5. loss of fxn
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11
Q

Chronic Inflammation

A

when inflammation persists past an amount of normal tissue time needed to resolve
Main cells = macrophages and lymphocytes
- they replace neutrophils ~ 48 hours post infection or injury

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12
Q

“Secondary tissue injury”

A

inadvertent injury to normal cells due to unregulated inflammation (like autoimmune conditions or allergic reactions)

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13
Q

What are the two main cellular receptors associated with Acute Inflammation?

A
  1. Toll-like receptors

2. Inflammassomes

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14
Q

Toll-like receptors

A

within sentinel cell’s plasma membrane and detect infectious pathogens–> then secrete pro-inflammatory cytokines

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15
Q

Inflammasomes

A

within sentinel cell’s cytosol and detect molecules associated with cellular injury/damage (extracellular DNA and ATP, uric acid from DNA break down, or amyloid proteins) –> then secrete cytokines

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16
Q

Inflammatory stimuli

A

infections microbes, necrosis, foreign bodies

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17
Q

Foreign bodies

A

shrapnel (grenade fragments, splinters, sutures,etc. that are traumatically introduced

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18
Q

What does acute inflammation begin with?

A

changes to blood vessel walls that allows fluid, plasma proteins and leukocytes to leave circulation and move toward target tissue

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19
Q

Vascular Changes ass. with acute inflammation

A

begin with vasoconstriction–> quick, lasts few seconds
transitions to prolonged vasodilation –> therefore vessel walls are more permeable (so intravascular fluid and plasma proteins more through vessel wall)

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20
Q

Three Mechanisms to Increase Vessel Wall Permeability

A
  1. Endothelial Cell Contraction
  2. Endothelial Injury
  3. Angiogenesis
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21
Q

Endothelial cell contraciton (Ass. w/ Vessel Wall Permeability)

A

most common; “retraction of endothelial cells”; ind. endothelial cells squeeze down and produce gaps
- mediated by HISTAMINE

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22
Q

Endothelial injury (Ass. w/ Vessel Wall Permeability)

A

less common; continue until endothelial cells been repaired
Caused by: severe burns, severe infecitons, exposure to highly toxic substances
- Endothelial cell necrosis

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23
Q

Endothelial cell necrosis

A

may cause unregulated fluid loss in inds. with severe burns; when 20% body covere din 3rd or 4th degree burns and care not provided –> ind. at risk of lethal hypovolemia shock

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24
Q

Angiogenesis (Ass. w/ Vessel Wall Permeability)

A

formation of new blood vessels– do NOT have mature vessel walls yet and therefore increase permeability; common at site of tissue repair and hallmark feature of tumor growth

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25
Edema
fluid that accumulates with increase vessel wall permeability
26
Exudate
protein-rich form of edema at site of ACUTE inflammation; no pitting Ex: sprained ankle
27
Transudate
protein-poor form of edema; with non-inflammatory processes; produces "pitting edema" Ex: congested heart failure
28
How do leukocytes get recruited, related to vessel walls?
increase in vessel wall permeability = fluid leaves vessels = decrease fluid content of blood = blood becomes MORE viscous and flows slower at site of ACUTE inflammation--> pushes larger WBC's to wall and RBC's to enter
29
Steps of WBC exiting vessel
1. Margination 2. Rolling 3. Firm adhesion
30
Margination
process of WBC's accumulating near vessel wall
31
Rolling
WBC's roll along vessel wall; mediated by SELECTINS
32
Firm Adhesion
WBC's stop moving and tightly bond onto inside vessel wall; mediated by INTEGRINS
33
Lymphangitis
acute inflammatory reaction is within the lymphatic vessels; almost always result of microbial infection after trauma
34
Lymphadenopathey
general term; for a disease affecting the lymph nodes
35
Lymphadenitis
a lymph node is inflammed and commonly associated with increase in size and pain upon palpation
36
Opsonization
"coating" or "tagging" microbes or cellular debris with an opsonin (greatly enhances phagocytosis); adheres immunoglobulins (antibodies) or complement proteins to outside wall of infections microbes or injured tissues
37
Phagosome
what target is engulfed into by pseudopodia
38
Phagolysome
binding of phagosome lysosomes; and breaks down its contents by exposing to bursts of ROS and lysosomal enzymes
39
Leukocyte-Induced Tissue Injury or Secondary Tissue Injury
when leukocytes injure normal cells and harmful to body; may occur as collateral damage to tissue surrounding acute inflammation reaction ; leukocytes are indiscriminate
40
What three situations cause Leukocyte-induced Tissue injury?
1. Persistent Infections 2. Ischemia-Reperfusion injuries 3. Hypersensitivity Reactions
41
Factors that influence outcome of acute inflammation (4)
1. nature of injury (i.e burn vs infection) 2. severity of injury 3. tissue(s) being injured 4. Host's responsiveness of injury --> ex. age
42
What are the three main outcomes of Acute inflammation?
1. Resolution 2. Chronic Inflammation 3. Fibrosis (scarring)
43
Resolution outcome of acute inflammation
"complete resolution" or tissue "regeneration"; reestablishing tissue to state indistinguishable from pre-injury status; injured cells must be able to replicate (divide); most likely occurs in mild, limited, and injuries involving minimal tissue Ex: paper cut or an aphthous ulcer
44
Fibrosis outcome of acute inflammation
(=scarring); occurs following sig. tissue injury or in cells with NO ability to divide or repair; chronic inflammation often transitions into this
45
Scar tissue
= non functional tissue anc cannot perform functions of cells it replaced
46
Examples of Fibrosis
- liver cirrhosis and loss of metabolic activity - scars on skin and decrease elasticity and strength - survive heart attack and decrease cardiac contractability and develop heart failure
47
Six Morphological Patters of Inflammation
1. Serous Inflammation 2. Fibrosis Inflammation 3. Purulent Inflammation 4. Ulcerative Inflammation 5. Pseudomembranous Inflammation 6. Granulomatous Inflammation
48
Serous inflammation
``` involves serum (serous fluid) accumulating within spaces b/w epithelial cells or within body cavities; commonly triggered by viral infections, burns, or autoimmune rxns - NOT infected and does NOT contain large amounts of leukocytes Ex: blister ```
49
Large and small blister
``` vesicle = smaller blister bulla = large blister ```
50
Fibrosis inflammation
occurs when high levels of inflammation cause a large increase in vessel wall permeability to point where large molecules (like fibrinogen) move outside of vessel lumen and become deposited on inflamed tissue
51
What is fibrosis commonly triggered by?
inflammation on body cavities; pericardium, pulmonary pleura, or meninges Examples: - survive heart attack and fibrinogen leaves circulation and deposits on inside of pericardium --> overtime will lead to scarring--> adds friciton to beating of heart--> accelerate heart failures
52
Purulent Inflammation
AKA suppurative inflammation; occurs when pus is present at site of acute inflammation; most likely indicates that pyogenic bacteria have infected tissue
53
Pus
collection of liquefied cellular tissue, protein-rich exudate, and several leukocytes (like neutrophils)
54
Pyogenic
pus-forming
55
Abscess
a localized collection of pus
56
Ulcerative Inflammation
development of an ulcer, which is a local tissue defect on surface of tissue or organ; superficial cells slough off following tissue necrosis Examples: - canker sore (aphthous ulcer) affects ~ 50% pop. - peptic ulcer disease, diabetic ulcers, or pressure ulcers (bed sores)
57
Pseudomembranous Inflammation
infections microbe secretes a necrotizing toxin that causes necrtoic tissue and WBC's to accumulate on surface Example: - present in tonsils of patients with diphtheria - present in colon of patients with pseudomembranous colitis
58
Granulomatous Inflammation
pattern of CHRONIC inflammation; a collection of macrophages, and some T-cells, and may have central region of necrosis; usually develops due to presence of foreign bodies or persistent immune reaction - associated with tuberculosis Also present in: Crohn's disease, sarcoidosis, syphilis, leprosy, persistent fungal infections, and cat-scratch disease
59
Noncaseating granuloma
commonly used to indicate the granulomatous inflammation is unlikely to be from tuberculosis
60
Granuloma
a site of granulomatous inflammation; descirbed as a "giant cell" or Langhans giant cells b/c marcophages pack together; also described as epitheloid cells b/c the collection of macrophages also described as rambling layered appearance of epithelial cells
61
Pain and Acute Inflammation is signaled by what two things?
1. Prostaglandins | 2. Substance P
62
Prostaglandins
produced by mast cells, macrophages, and endothelial cells--> signal pain and fever
63
Fever
any body temp above normal 98.6 F (37 C); most common greater than 100.4 F (38 C); produced when prostaglandins interact with hypothalamus to increase body's temp. set point
64
Substance P
is a neuropeptide (NT) produced by various leukocytes and sensory neurons - involved with transmission of pain signals
65
What does suffix "-oid" mean?
means resembling something else
66
Two main processes of tissue repair
1. Regeneration | 2. Fibrosis (scarring)
67
Regeneration
when tissues return to a "pre-injury" state; involves growth (proliferation) of uninjured cells at area of inflammation; ONLY possible if normal tissue not obliterated and is regular dividing or high capacity for cell division
68
Examples of tissue that can regenerate
skin or gastrointestinal mucosa Hepatocytes--have unique ability to regenerate; after partial heptectomy the liver may regrow to normal size following up to 90% of its mass
69
Fibrosis (scarring)
involves deposition of fibrous connective tissue-- collagen fibers; during tissue repair; serves as a "patch" rather than restoring normal tissue structure and function; occurs in tissue incapable of dividing or follow severe tissue damage
70
Examples of tissue that undergoes fibrosis
cardiac myocytes, skeletal muscle, or CNS neurons, lungs, kidneys and any tissue following severe tissue damage (i.e. severe abrasion)
71
What is the relationship between damage to ECM and scarring?
Increase damage to ECM; increase scarring
72
Fibroblasts
are recruited to site within 3-5 days by macrophages being alternatively activated and secrete growth factors and stimulate new blood vessel formation and recruit the fibroblasts
73
Steps in Scar Formation
1. angiogenesis 2. fibroblast migration and proliferation 3. collagen deposition --> scar 4. remodeling (occurs over lifetime)
74
Matrix Metallopretoeinase (MMPS)
breakdown tissue--collagen; they are produced by: fibroblasts, macrophages, neutrophils, and epithelial cells Cofactor = zinc ion
75
Keloids
scarring beyond boundaries of wound; excessive granulation tissues and excessive collagen; raised and flesh colored lesion; won't regress and if remove it comes back worse
76
Where can keloids occur?
any cutaneous surface; injury to dermis increase risk - possible pain or itching - more common in African Decent Ex: Cauliflower Ear
77
Cauliflower Ear
irregular collagen formation; auricular hemotoma; trauma disrupts blood vessels; shearing forces seperate anterior perichondrium from the underlying cartilage
78
Treatment for Cauliflower ear
drainage within 7 days
79
Factors influencing repair
1. infection 2. nutritional deficiency 3. gluccorticoids (steroids) 4. poor perfusion 5. Etc. increase age; mechanical pressure/distortion, anemia, foreign bodies, UV light
80
The Phases of healing skin wounds
1. inflammation 2. formation of granulation tissue (3-5 days) 3. ECM deposition and remodeling (all overlap)
81
What 4 things does Chronic Inflammation develop from
1. Persistent infection 2. prolonged injury 3. hypersensitivity reactions 4. immunosuppression
82
Persistent infection (leading to chronic inflammation)
some infectious microbes = difficult to eradicate | Examples: Hepatities B and C, tuberculosis, or Clostridium difficile (C-Diff)
83
Prolonged Injury (leading to chronic inflammation)
may be do to daily exposure that continually causes injury to tissue Examples: -tobacco smoke cont. injury respiratory tract and cause chronic bronchitis - harness that continually rubs
84
Hypersensitivity reactions (leading to chronic inflammation)
involve allergies and autoimmune conditions
85
Immunosuppression (leading to chronic inflammation)
inadequate immune response (may allow inf. to persist longer); ass. with age related redcutions in immune function Examples: - AIDS - medically- induced in ind. receiving tissue/organ transplant
86
Cells involved with chronic imflammation
macrophages*, lympocytes (T cells, B cells, NK cells), and plasma cells
87
Classically Activated Macrophages
perform phagocytosis of microbes and cellular debris; secrete cytokines--> promote cont. inflammation
88
Stimuli that activate Classically Activated Macrophages
microbes, crystalline substances, or particles from tissue necrosis
89
Alternatively Activated Macrophages
secrete Growth Factors and stimulate repair by increase angiogenesis and recruit fibroblasts
90
Fibroblasts
cells that secrete collagen and found at CHRONIC inflammation when scar tissue deposition occuring or about to occur
91
Angiogenesis
ingrowth of new blood vessels; also body's way to attempt to heal area
92
Systemic Effects of Inflammation
1. Fever 2. Acute-phase proteins 3. Leukocytosis 4. Leukemoid Reactions 5. other effects of acute-phase reaction--anorexia, somnolence, and malaise
93
Acute-phase proteins
1. C-Reactive Protein (CRP) | 2. Erythrocyte Sedimentation rate (ESR)
94
C-Reactive Protein (CRP)
are elevated in inflammation response, (nonspecific lab findings for inflammation); increase CRP levels is a marker for heart attack risks; progression of coronary artery disease
95
Erythrocyte Sedimentation Rate (ESR)
the rate that RBC's fall out of suspension with in 1 hour (nonspecific test, marker for body-wide inflammation) - Fibrinogen brins RBC's together and increase ESR (increase fibrinogen proteins, ass. with increase inflammation, and increased ESR)
96
Leukocytosis
elevated WBC inside ciruclation Normal Range = 4,000 - 10,000 cells per microliter Leukocytosis = 15,000-30,000
97
Bacterial infections are more likely to produce elevation of what cells? Viral infections?
bacterial infections--> elevated neutrophils | viral infections--> elevated lymphocytes
98
Leukemoid reactions
``` extremely elevated WBC counts 40,000-100,000 cells per mL Mimic elevate WBC levels ass. with leukemia Conditions that produce this: - infectious mononucleosis ("Mono") - tuberculosis - C-Diff infection ```

General Pathology -- Roecker (7 decks)

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