Lecture 13 Flashcards

1
Q

Dolar

A

Pain

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2
Q

Calor

A

Heat

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3
Q

Rubor

A

Redness

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4
Q

Tumor

A

Swelling

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5
Q

What is the effects of acute inflammation?

A

Release of chemical mediators (histamine, kinins, prostaglandins) -> vasodilation (hot, red), Irritation of nerve endings (pain), increased capillary permeability (edema, pain) (-> clot, fibrin mesh walls of area), chemotaxis (WBC to area) (-> phagocytosis)

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6
Q

What allows for preparation for healing?

A

Clot formation, phagocytosis

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7
Q

What are the forms of healing?

A
  1. Scar tissue (fibrosis)
  2. Regeneration (Irreversible damage)
  3. Resolution (Reversible damage)
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8
Q

Mast Cells

A

Tissue cell from basophils; Cells that release mediators during allergic reactions

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9
Q

Plasma Cells

A

Tissue cell from lymphocytes; Differentiated B cell that produces antibodies

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10
Q

Macrophage

A

Tissue cell from monocytes; large phagocytic cells that engulfs and digests cell debris and pathogens

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11
Q

Polymorphonuclear Neutrophil

A

Inflammatory cell; Type of WBC (first responder to infection

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12
Q

Eosinophil

A

Inflammatory cell; WBC involved in parasitic infections and allergic reactions

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13
Q

Basophil

A

Inflammatory cell; releases histamine during allergic reaction

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14
Q

Monocyte

A

Inflammatory cell; differentiates into macrophages and dendritic cells

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15
Q

Lymphocyte

A

Inflammatory cells; adaptive immunity (B cells and T cells)

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16
Q

Platelet

A

Cell fragments involved in clotting and wound healing

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17
Q

Granulocytes

A

WBCs that contain granules in their cytoplasm (neutrophils, eosinophils, basophils)

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18
Q

Agranulocytes

A

WBCs that do not contain granules (lymphocytes and monocytes)

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19
Q

Azurophilic Granules

A

Granules that are found in certain leukocytes that contain enzymes and antimicrobial substances

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20
Q

What types of granules and substrates are found in neutrophils?

A
  1. Specific granules: phospholipase A, elastase, cathepsin
  2. Azurophilic Granules: phospholipase A, Type IV collagenase
  3. Tertiary Granules
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21
Q

What types of granules and substrates are found in eosinophils?

A
  1. Specific: Histaminase, collagenase, cathepsins
  2. Azurophilic: collagenase
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22
Q

What types of granules and substrates are found in basophils?

A
  1. Specific: histamine, synthesis of leukotriene
  2. Azurophilic
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23
Q

Phospholipase A

A

enzyme that releases arachidonic acid from phospholipids (production of eicosanoids)

24
Q

Cathepsins

A

Group of proteases involved in protein degradation within lysosomes

25
Type IV Collagenase
Enzyme that degrades type IV collagen
26
Histaminase
Enzyme that degrades histamine to modulate allergic reactions
27
Collagenase
enzyme that breaks down collagen
28
Leukotriene
Type of eicosanoid
29
Erythrocyte Sedimentation Rate
Blood test that is used for inflammation
30
Kinins
Peptides that cause vasodilation, increased vascular permeability and induce pain Bradykinin: inflammatory response
31
Arachidonic Acid Derivative
- Inflammatory mediators -Synthesis inhibited by steroids, NSAIDs, COX-inhibitors
32
COX1
-Inhibit COX production - Constitutive - Physiological function involvement
33
COX2
-Inhibit COX production - Inducible -Inflammatory sites
34
IFN-alpha
Interferon involved in antiviral response and regulation of immune functions
35
IFN-gamme
Cytokine that enhances immune response and activates macrophages
36
Non-Steroidal Anti-Inflammatory Drugs (NSAIDs)
Medications that decrease inflammation, pain, fever by inhibiting COX enzymes involved in the production of prostaglandins
37
Risk of COX inhibition by NSAIDs
Gastric ulcers, renal ischemia, premature closure of ductus arteriosus (fetal blood vessel), Reye's syndrome
38
Prostaglandin E2 (PGE2)
Promotes inflammation, pain, fever
39
Synoviocytes
Cells that line synovial membrane of joins
40
Thromboxane (TXA2)
Prostaglandin derivative produced primarily by platelets (promotes vasoconstriction and platelet aggregation)
41
Prostacyclin (PGI2)
Prostaglandin produced by endothelium that acts as vasodilator and inhibitor of platelet aggregation
42
COX2 Specific Inhibitors
- Capitalize on anti-inflammatory and pain relieving properties of NSAIDs while bypassing risks with COX1 inhibition - Risks: myocardial infarction (prothrombotic effects via inhibition of endothelial function) -> decrease antithrombotic PGI2 with no inhibition of prothrombotic platelet TXA2
43
Prothrombotic
Condition that promotes thrombosis (Blood clot formation)
44
What factors can cause edema?
1. Increased venous pressure 2. Decreased oncotic pressure of plasma resulting from decreased albumin 3. Increased permeability of vessel wall 4. Obstruction of lymphatics
45
Albumin
Plasma protein synthesis in liver (oncotic pressure on transport control)
46
What cells can undergo phagocytosis?
Neutrophils and macrophages
47
Macrophage-Derived Interleukin-1
Stimulates release of neutrophils from bone marrow storage (neutrophilia)
48
Toll-Like Receptor (TLR)
First receptors activated during host-pathogen interaction (CD-14 coreceptor: detects bacterial LPS)
49
C-Reactive Protein (CRP)
Acute phase protein produced by liver in response to inflammation
50
Serum Amyloid-A
Acute phase protein that increases inflammation
51
Tumor Necrosis Factor Alpha (TNF-A)
Cytokine involved in systemic inflammation
52
Why do fevers occur?
Cytokines act on endothelial cells of highly vascularized organum vasculosum laminae terminalis (OVLT) -> OVLT signals -> vasoconstriction of dermal vessels -> cessation of sweating and shivering of muscles -> decreased dissipation of heat -> PGE2 diffuses into hypothalamus -> increases set point for thermoregulation
53
Organum Vasculosum Laminae Terminalis (OVLT)
Specialized brain region involved in thermoregulation
54
Primary Intention Scar
Composition of matrix changes from fibronectin and fibrin -> collagen III -> collagen type I
55
Secondary Intention Keloid
Excessive scarring causes formation of keloid
56
Keloid
Scar composed of type III collagen (not type I)
57
Granulation tissue
temporary/make-shift structure (fibrous CT that replaces fibrin clot in healing tissue)