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Pathology > 1c continued > Flashcards

1c continued Flashcards

1
Q

Chemical mediators general overview a 4 groups according to function

A

All S&S of inflammation are produced by chemical mediators
1 vasoactive properties
2 activate complement (clotting and kinin)
3 Chemotactic factors
4 Direct affectation of tissue cells

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2
Q

Histamine

A

Found preformed in mast, basophils and platelets.
Released from trauma or immune reactions (IgE binding)
First on scene
Binds to H1 (antihistamines often competitively antagonize H1)
Causes dilation of arterioles, and increases permeability of venules.
Considered principle mediator of immediate transient phase of increased vascular permability

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3
Q

Histamine H1 receptors specifically

A

-Promote inflammation from vasodilation, increased vascular permeability (due to retraction of endothelial cells lining caps)
-Chemotaxis
-Prostaglandin synthesis
Smooth muscle effects are bronchoconstriction and vasodilation

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4
Q

Histamine H2 receptors functions

A

Negative feedback (decrease histamine release) which reduces activity of lymphocytes and eosinophils, decreases neutrophil chemotaxis, decrease granulation of mast cells

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5
Q

H2 location

A

Parietal cells of stomach mucosa which increase gastric secrtion

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6
Q

Arachidonic acid two pathways

A 
It is found in phospholipid bilayers and released by phospolipase A2. Release leads to
Cyclooxygenase pathway (prostaglandins and thromboxane) 
Lipoxygenase pathway (leukotrienes)
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7
Q

Leukotrienes effects and pathway

A

Similar to histamine
Constricts pulmonary airway
Increase microvascular permability
From AA to lipoxygenase to leukotriens)

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8
Q

Prostaglandins

A

Promotes and inhibits inflammation cell response
Induces vasodilation
Induces vasoconstriction
From AA to cyclooxygenase

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9
Q

Thromboxane

A

From AA to cylcooxygenase pathway

Promotes platelet aggregation, vasodilation, bronchoconstriction

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10
Q

Arachadonic acid metabolites

A

Lipoxygenase (leukotriene receptor antagonist) Leukotrienes

Cyclooxygenase (asprin NSAID) prostaglandin and thrombaxane

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11
Q

Platelet Activating Factor

A

Lipid stored in membranes, induces platelet aggregation, activates neutrophils, chemotactic factor eosinophils

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12
Q

Plasma Proteins Three interrelated systems

A

Clotting, complement, and kinin

Inactive and need to be triggered

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13
Q

Clotting Cascade plasma proteins

A

Produces chemokines, expression of endothelial adhesion molecules, prostaglandin synthesis
Thrombin binds to PARs which triggers production of these plus PAF

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14
Q

Complement system plasma proteins

A

Contribute by causing vasodilation, increasing vasc permeability, enhancing phagocyte activity, and forms Membrane Attack Complex MAC

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15
Q

Kinin System plasma proteins

A

Release of bradykinin:
Increased vasc perm
Smooth muscle contraction
Vasodilation and incites pain when bound to nociceptors

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16
Q

Cytokines

A

Proteins produced by many different cells which cause functional effects on other cell types
Examples tumor necrosis factor-a and interleukin-1
They are released by macrophages and cause a wide range of effects
There are several forms of interleukins

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17
Q

Chemokines

A

Chemotactic cytokines

They are proteins that attract leukocytes and other inflammatory cells to site of injury

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18
Q

Nitric oxide

A

Smooth muscle relaxation, platelet antagonism, reduction of leukocyte recruitment
Can be considered a mechanism that prevents cell stage of inflammation from going too far
Produced by many cells

19
Q

ROS

A 
Produced during phagocytosis, released exogenously
Exogenous effects of ROS:
Increased vasc perm
Increased endothelial adhesion
Increasion expression of cytokines
20
Q

Exudates

A

Serious - watery fluids low in protein, a result of large amounts of plasma
Hemorrhagic - caused by vessel damage, or increased leaking of RBCs into tissue
Fibrinous - large amounts of fibrinogen (similar to a clot)
Membranous - develop on mucous membranes
Purulent - contains pus (degraded WBCs, proteins, tissue debris)

21
Q

Abscess

A

Localized inflammation with purulent (pus) exudate
Has a central necrotic core surrounded by a layer of neutrophils
POSSIBLY surronded by a layer of fibroblasts which would prevent anti-microbial agents from entering
This is why you often see abscess’ drained

22
Q

Ulceration

A

Localized inflammation with epithelial damage
Erosion of tissue
From trauma or vasc deficits

23
Q

Chronic inflammation

A 
2 weeks + 
Not self-limiting, self-perpetuating
caused by:
recurrent acute inflammation
progressive acute
persisten low grade irritants
24
Q

Chronic inflammation is charactrized by

A

Influx of macrophages and lymphocytes as opposed to neutrophils in acute response
By build up of fibroblasts rather than exudate which leads to risk of scarring

25
Q

Nonspecific inflammation

A

Diffuse accumulation of macrophages and lymphocytes
Continual chemotaxis
fibroblast proliferation
scar formation

26
Q

Granulomatous inflammation

A

Mass of macrophages surrounded by lymphocytes
Insulting agent was poorly controlled by other inflam mechs
CT eventually encapsulates mass
Example would be TB

27
Q

Systemic manifestations

A 
Body tries to control inflammation to local, if it does go systemic it is characterized by THREE features
Acute-phase response
WBC response
Lymphadenitis (swollen members)
Severe systemic is cytokine storm
28
Q

Acute phase response

A 
From cytokines systemic
Increased C reactive protein*
Eleveated CSR*
Skeletal muscle catabolism
Negative nitrogen balance
Fever, anorexia, somnolence, malaise
29
Q

WBC response in systemic

A

Bacterial infections produce increase in neutrophils
Parasitic and allergic responses produce increase in eosinophils
Viral infections produce decrease in neutro increase in lymphocytes

30
Q

Leukocytosis

A

increased WBC

decreased is leukopenia

31
Q

Lymphadenitis

A

Lymphs responsible for draining inflammation
Either due to immunologic response to specific antigen or a generalized response to chemical medatiors in the inflammation

32
Q

Cytokine storm

A

Massive release of chemical mediators into body SIRS

33
Q

Tissue repair

A

Tissue regen - replacement with same cells

Fibrous tissue - replacement with CT (scar)

34
Q

Healing is regulated by

A

chemical mediators, ECM, and growth factors

35
Q

Growth factors

A

Hormone-like molecules interact with specific cell receptors, control proliferation, differentiation, metabolism of cells during healing process
Also regulate inflammatory process, act as chemo attractants, stimulate angiogensis, help form ECM

36
Q

Cells involved in wound healing

A 
Leukocytes
Macrophages
Epithelial cells
CT (myofibros, angio, and fibro -blasts)
Tissue rich in those ^ is granulation tissue
37
Q

Primary vs secondary intention

A

Small close wounds heal by primary

Large spaced out ones are secondary

38
Q

3 phases of wound healing

A

Inflammatory
Proliferative
Remodeling

39
Q

Inflammatory phase of healing

A

Prepares environment

Needs proliferation of chem mediators and growth factosr

40
Q

Proliferative Phase

A

Formulation of granulation tissue (fibro, myofibro, angioblasts)
Epithelization also occurs (migration, prolif, and differentiation of epithelial cells at wound edges to form new layer)

41
Q

Remodeling phase of wound healing

A

Type 3 collagen replaced with Type 1, done to increase overall strength of wound

42
Q

Factors affecting wound healing

A 
Nutrition
Blood flow
Impaired inflammatory or immune resonses
Infecction
Wound seperation
Foreigners
43
Q

Complications of bad wound healing

A 
Loss of founction
Contractures (perm shortening of muscle or joint) and obstruction
Adhesions
Hypertrophic scar tissue (keloid -elevated scars) 
Ulcerations
Wound dehiscence
Infection
Delayed healing

Pathology (24 decks)

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