Inflammation and Repair (Schoenwald) Flashcards

(52 cards)

1
Q

In degeneration, what are two reversible cellular responses to injury?

A

1) Cellular swelling (proteinaceous)
2) Fatty degeneration (fatty change in organ or cell, steatosis: i.e. fatty liver)

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2
Q

Define atrophy

A

Catabolic metabolism of cell, not immediately lethal to cell. Cell/organs shrink with or w/o accumulation of metabolic products

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3
Q

What can cause symmetric atrophy?

A

Old age

Reduced blood supply

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4
Q

Causes of asymmetric atrophy

A
  • Decreased workload
  • Nutritional deficiencies
  • Neuro endocrine
  • Chronic low-level injury (radiation, chemical toxins)
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5
Q

What is defined as symmetric atrophy of the entire body? (Can be caused by tumors, AIDs, TB)

A

Cachexia

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6
Q

What are two major purposes of apoptosis (programmed cell death)? What cell type is involved in the “clean up” after apoptosis?

A

1) natural cell turnover in development and aging
2) disposal of damaged or dysfunctional cells
- Macrophages clean up degraded cellular material

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7
Q

What process follows irreversible cell and tissue injuries?

A

Necrosis

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8
Q

What is the difference between coagulative necrosis and liquefaction necrosis?

A

Coagulative: tissue with normal protein content

Liquefaction: tissue poor in protein (brain and fat)

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9
Q

Autolysis involves ____-digestion, while ______ involves digestion of adjacent cells and tissues by enzymes released from ________ cells.

A

Autolysis involves self-digestion, while heterolyis involves digestion of adjacent cells and tissues by enzymes released from dying cells.

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10
Q

5 common causes of necrosis

A

1) Ischemia
2) Trauma
3) Toxin
4) Infection
5) Immunologic factors

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11
Q

Local changes of inflammation include _______ and ________ _________.

A

Local changes of inflammation include vasodilation and vascular permeability.

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12
Q

________ is the process that allows for WBC accumulation at the site of injury/inflammation.

A

Chemotaxis

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13
Q

Acute inflammation:

1) onset and duration
2) characterized by _______ fluid and ________
3) main cell type involved

A

Acute inflammation:

1) rapid onset, lasts minutes to days
2) characterized by exudative fluid and protein
3) Neutrophils are main cells involved

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14
Q

What are the 4 cardinal signs of acute inflammation?

A

1) Rubor- redness
2) Calor- heat
3) Dolor- pain
4) Tumor- mass effect

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15
Q

What are 6 causes of acute inflammation?

A

1) infection
2) trauma
3) physical/chemical agents
4) necrosis
5) foreign bodies
6) immune reactions

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16
Q

What are 3 mediators released by cells in acute inflammation that cause vasodilation? How do they work?

A

Histamine, prostacyclin, nitric oxide

Increases hydrostatic pressure by slowing blood flow–> causing margination of leukocytes along the vessel wall

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17
Q

What cell mediators are released causing vascular permeability in acute inflammation?

A

Histamine and leukotrienes

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18
Q

Increased leakiness of vessels caused by release of histamine and leukotrienes allows fluid to cross interstitial tissues —> causing (increased/decreased) protein at interstitial tissue which causes (increased/decreased) osmotic pressure in blood and (increased/decreased) osmotic pressure in tissue.

==>Causing _____ of interstitial tissue

A

Increased leakiness of vessels caused by release of histamine and leukotrienes allows fluid to cross interstitial tissues —> causing increased protein at interstitial tissue which causes decreased osmotic pressure in blood and increased osmotic pressure in tissue.

==>Causing edema of interstitial tissue

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19
Q

What are 5 mechanisms of increased vascular permeability?

A

1) endothelial contraction (short lived)
2) endothelial retraction (long-lived)
3) direct endothelial injury
4) Delayed prolonged response (UV light, xray, mild thermal injury)
5) leukocyte mediated damage

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20
Q

In endothelial contraction, what mediators are involved and what is their MOA?

A

Endothelial contraction:

Histamine, bradykinin, and leukotriene mediated

MOA: acts on postcapillary venules

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21
Q

TNF and interleukin are mediators in what type of mechanism of increased vascular permeability? What is their MOA?

A

Endothelial retraction

MOA: structural rearrangement of cytoskeleton

22
Q

What mediates direct endothelial injury in order to increase vascular permeability? What vessels are affected and what is the MOA?

A

Direct endothelial injury:

Bacterial enzyme mediated

ALL vessels are affected

MOA: endothelial cell necrosis

23
Q

What are 3 types of movement of WBCs from blood vessels to the site of inflammation?

A

1) Rolling: loose, intermittent contact of WBC with endothelium. Due to margination of WBC from stasis of blood
2) Pavementing: tight, constant contact of WBC with endothelium
3) Transmigration: WBC cross through endothelial layer. Platelet cell adhesion molecule mediated

24
Q

Leukotrienes and IL-8 are exogenous/endogenous mediators while bacterial polysaccharides are exogenous/endogenous mediators in chemotaxis.

A

Leukotrienes and IL-8 are endogenous mediators while bacterial polysaccharides are exogenous mediators in chemotaxis.

25
\_\_\_\_\_\_\_\_ are particles that bind to foreign material for WBC recognition. What are 3 mechanisms they use?
**Opsonins** 1) IgG-FC receptor site recognition on WBC 2) C3b (complement) 3) Collectins
26
Leukocytes recognize foreign particles through _______ detection and _________ receptors.
Leukocytes recognize foreign particles through **_mannose_** detection and **_scavenger_** receptors.
27
What are 2 mechanisms WBCs use to kill foreign substances? What chemical substances are involved?
1) **Reduced NADPH oxidase:** uses 2 oxygen molecules to produce superoxide radical which then converts to hydrogen peroxide --\> kills bacteria 2) **Myeloperoxidase**: converts hydrogen peroxide and halogen (Cl-) to HOCl which causes lipid or protein peroxidation --\> breaks down bacterial/invader cell wall
28
3 types of acute inflammation
1) serous inflammation 2) fibrinous inflammation 3) purulent inflammation
29
\_\_\_\_\_\_\_\_ inflammation is typically seen in viral infectons and burns while _________ inflammation is seen with bacterial and fungal infections.
**_Serous_** inflammation is typically seen in viral infectons and burns while **_Purulent_** inflammation is seen with bacterial and fungal infections.
30
What are some characteristics of serous inflammation?
**Serous inflammation:** - relatively clear, watery fluid - Transudative- few cells, protein poor, specific gravity \<1.012 - Viral infections and burns
31
What are characteristics of fibrinous inflammation?
**Fibrinous inflammation:** - finely particulate, thick fluid - exudative- protein-rich fluid, specific gravity \>1.020 - postmyocardial infarction pericarditis
32
What are characteristics of purulent inflammation?
**Purulent inflammation:** - Pus - neutrophil, protein-rich exudative - bacterial and fungal infections
33
What is the term for a walled off collection of pus that can occur in any organ?
Abscess
34
What are the 4 microscopic layers involved in ulcers?
From superficial to deep: - fibrin - neutrophils - granulation tissue - fibrosis
35
What is a fistula? How does it relate to inflammation?
A connection between 2 organs (typically organs with a lumen, i.e. colon, bladder) -inflammatory process involving full thickness wall of an organ, duct or blood vessel can lead to a fistula. The wall adheres to adjacent organ wall which allows for communication between the two organs
36
Chronic inflammation results in proliferation of new _______ and \_\_\_\_\_\_\_\_\_, production of \_\_\_\_\_\_\_\_\_\_, which leads to \_\_\_\_\_\_\_\_\_\_.
Chronic inflammation results in proliferation of new **_capillaries_** and **_fibroblasts_**, production of **_collagen_**, which leads to **_scarring_**.
37
Acute inflammation is more **(neutrophil/leukocyte)** mediated and chronic inflammation is **(neutrophil/leukocyte)** mediated.
Acute inflammation is more **neutrophil** mediated and chronic inflammation is **leukocyte** ​mediated.
38
Lymphohistiolytic infiltration with increasing fibroblast activity are associated with what type of inflammation? What type of tissue does this typically develop into?
Chronic inflammation lymphohistiolytic infiltration with increasing fibroblasts--\> **granulation tissue**
39
Granuloma formation may result from what type of mediated response in chronic inflammation?
T-cell immune response--\> granuloma formation (i.e. TB)
40
What are 4 causes of chronic inflammation?
1) viral 2) persistent microbial infection 3) prolonged exposure to toxin 4) autoimmune dysfunction
41
Proteases, IL-1, TNF, arachidonic acid metabolites, and nitric oxide (NO) are produced by what type of cells in chronic inflammation?
Activated macrophages
42
What is a collection of activated macrophages called? These are seen in response to TB, fungal infections, sarcoidosis, foreign materials, and silica exposure
Granulomatous inflammation (granuloma)
43
44
What is the difference between regeneration and healing?
**Regeneration:** complete replacement of damaged cells- NO scar formation. Can occur is skin, GI tract, compensatory tissue of liver and kidney **Healing:** regeneration of cells combined with scarring and fibrosis
45
What are 5 growth factors involved in repair?
1) epidermal growth factor 2) vascular endothelial growth factor 3) platelet derived growth factor 4) fibroblast derived growth factor 5) transforming growth factor -B
46
Match the growth factor with its function: ## Footnote **1) Epidermal growth factor, 2) Vascular endothelial growth factor, 3) Platelet derived growth factor, 4) Fibroblast derived growth factor, 5) Transforming growth factor -B** a: stimulates blood vessel formation and wound repair through macrophages, fibroblast, and endoethelial cell migration b: induces blood vessel formation c: acts as growth inhibitor for epithelium d: stimulates granulation tissue formation e: promotes migration and proliferation of smooth muscle cells
**1) Epidermal growth factor-** d: stimulates granulation tissue formation **2) Vascular endothelial growth factor-** b: induces blood vessel formation **3) Platelet derived growth factor-** e: promotes migration and proliferation of smooth muscle cells **4) Fibroblast derived growth factor-** a: stimulates blood vessel formation and wound repair through macrophages, fibroblast, and endoethelial cell migration **5) Transforming growth factor -B-** c: acts as growth inhibitor for epithelium
47
What are 4 requirements of replacement by a scar?
1) angiogenesis 2) migration and proliferation of fibroblasts 3) deposition of extracellular matrix 4) maturation and reorganization of fibrous tissue
48
Time frame for a scar: \_\_\_\_\_\_ = granulation tissue \_\_\_\_\_\_\_\_ = collagen deposition continues \_\_\_\_\_\_= inflammatory infiltrate absent and collagen starts to strengthen
Time frame for a scar: **_3-5 days_** = granulation tissue **_Week 2_** = collagen deposition continues **_1 month_** = inflammatory infiltrate absent and collagen starts to strengthen
49
Healing by **_(_primary/secondary)** intention involves healing of a wound with clean edges, close margins, and minimal tissue disruption. This leaves a **(small/large)** scar.
Healing by **_primary_** intention involves healing of a wound with clean edges, close margins, and minimal tissue disruption. This leaves a **_small (to nonexistent)_** scar.
50
Healing by (**primary/second)** intention involves a wound with unclean edges, extensive tissue disruption and necrosis. It results in a **(small/large)** scar. Debridement is usually necessary for healing.
Healing by **_second_** intention involves a wound with unclean edges, extensive tissue disruption and necrosis. It results in a **_large or prominent_** scar. Debridement is usually necessary for healing.
51
**True/False:** A fully healed wound is just as strong as normal skin
**False:** Fully healed wounds will never be as strong. They are about 2/3rd the strength of normal skin
52
What are 5 factors that impair wound healing?
1) Nutritional deficiency (protein, Vit C) 2) Infection 3) Steroid therapy 4) Poor blood flow 5) Pressure