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RRCCPA Physiology/Pathophysiology I > Inflammation and Repair (Schoenwald) > Flashcards

Inflammation and Repair (Schoenwald) Flashcards

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
Q

________ are particles that bind to foreign material for WBC recognition. What are 3 mechanisms they use?

A

Opsonins

1) IgG-FC receptor site recognition on WBC
2) C3b (complement)
3) Collectins

26
Q

Leukocytes recognize foreign particles through _______ detection and _________ receptors.

A

Leukocytes recognize foreign particles through mannose detection and scavenger receptors.

27
Q

What are 2 mechanisms WBCs use to kill foreign substances? What chemical substances are involved?

A

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
Q

3 types of acute inflammation

A

1) serous inflammation
2) fibrinous inflammation
3) purulent inflammation

29
Q

________ inflammation is typically seen in viral infectons and burns while _________ inflammation is seen with bacterial and fungal infections.

A

Serous inflammation is typically seen in viral infectons and burns while Purulent inflammation is seen with bacterial and fungal infections.

30
Q

What are some characteristics of serous inflammation?

A

Serous inflammation:

  • relatively clear, watery fluid
  • Transudative- few cells, protein poor, specific gravity <1.012
  • Viral infections and burns
31
Q

What are characteristics of fibrinous inflammation?

A

Fibrinous inflammation:

  • finely particulate, thick fluid
  • exudative- protein-rich fluid, specific gravity >1.020
  • postmyocardial infarction pericarditis
32
Q

What are characteristics of purulent inflammation?

A

Purulent inflammation:

  • Pus
  • neutrophil, protein-rich exudative
  • bacterial and fungal infections
33
Q

What is the term for a walled off collection of pus that can occur in any organ?

A

Abscess

34
Q

What are the 4 microscopic layers involved in ulcers?

A

From superficial to deep:

  • fibrin
  • neutrophils
  • granulation tissue
  • fibrosis
35
Q

What is a fistula? How does it relate to inflammation?

A

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
Q

Chronic inflammation results in proliferation of new _______ and _________, production of __________, which leads to __________.

A

Chronic inflammation results in proliferation of new capillaries and fibroblasts, production of collagen, which leads to scarring.

37
Q

Acute inflammation is more (neutrophil/leukocyte) mediated and chronic inflammation is (neutrophil/leukocyte) mediated.

A

Acute inflammation is more neutrophil mediated and chronic inflammation is leukocyte ​mediated.

38
Q

Lymphohistiolytic infiltration with increasing fibroblast activity are associated with what type of inflammation? What type of tissue does this typically develop into?

A

Chronic inflammation

lymphohistiolytic infiltration with increasing fibroblasts–> granulation tissue

39
Q

Granuloma formation may result from what type of mediated response in chronic inflammation?

A

T-cell immune response–> granuloma formation (i.e. TB)

40
Q

What are 4 causes of chronic inflammation?

A

1) viral
2) persistent microbial infection
3) prolonged exposure to toxin
4) autoimmune dysfunction

41
Q

Proteases, IL-1, TNF, arachidonic acid metabolites, and nitric oxide (NO) are produced by what type of cells in chronic inflammation?

A

Activated macrophages

42
Q

What is a collection of activated macrophages called? These are seen in response to TB, fungal infections, sarcoidosis, foreign materials, and silica exposure

A

Granulomatous inflammation (granuloma)

43
Q
A
44
Q

What is the difference between regeneration and healing?

A

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
Q

What are 5 growth factors involved in repair?

A

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
Q

Match the growth factor with its function:

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

A

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
Q

What are 4 requirements of replacement by a scar?

A

1) angiogenesis
2) migration and proliferation of fibroblasts
3) deposition of extracellular matrix
4) maturation and reorganization of fibrous tissue

48
Q

Time frame for a scar:

______ = granulation tissue

________ = collagen deposition continues

______= inflammatory infiltrate absent and collagen starts to strengthen

A

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
Q

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.

A

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
Q

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.

A

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
Q

True/False: A fully healed wound is just as strong as normal skin

A

False: Fully healed wounds will never be as strong. They are about 2/3rd the strength of normal skin

52
Q

What are 5 factors that impair wound healing?

A

1) Nutritional deficiency (protein, Vit C)
2) Infection
3) Steroid therapy
4) Poor blood flow
5) Pressure

RRCCPA Physiology/Pathophysiology I (23 decks)

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