WorksheetsL3 - Pathology
Total questions: 42
Worksheet time: 7hrs 0mins
Inflammation is the reaction of vascularized living tissue to local injury. Cause of inflammation: Injurious stimuli
True
False
Identify the cardinal sign of inflammation:
• Redness
• Vasodilation and increased blood flow
Rubor
Calor
Dolor
Tumor
Function laesa
Identify the cardinal sign of inflammation:
• Heat
• Vasodilation and increased blood flow
Rubor
Calor
Dolor
Tumor
Function laesa
Identify the cardinal sign of inflammation:
• Pain
• Cytokines
• Category of signaling molecules that mediate and regulate immunity, inflammation, and hematopoiesis
Rubor
Calor
Dolor
Tumor
Function laesa
Identify the cardinal sign of inflammation:
• Swelling
• Local edema
Rubor
Calor
Dolor
Tumor
Function laesa
Identify the cardinal sign of inflammation:
• Loss of function
Rubor
Calor
Dolor
Tumor
Function laesa
Vasodilation leads to increased blood flow
True
False
Leukocyte extravasation in cellular phase of inflammation (M.R.A.D) (may isang impostor)
Margination
Rolling
Adhesion or pavementing
Diapedesis or transmigration
Destination
Bacterial infections
neutrophils
mononuclear cells (lymphocytes and monocytes)
eosinophils
Viral infections
neutrophils
mononuclear cells (lymphocytes and monocytes)
eosinophils
Allergic reactions
neutrophils
mononuclear cells (lymphocytes and monocytes)
eosinophils
Emigration of WBC’s neutrophils followed by lymphocytes
Extravasation
Chemotaxis
Phagocytosis
Unidirectional migration of WBC’s to the site of injury
Extravasation
Chemotaxis
Phagocytosis
Process by which foreign particles (bacteria) are ingested by the leukocytes. 4 Steps: Attachment, Engulfment, Fusion of lysosome, Killing
Extravasation
Chemotaxis
Phagocytosis
plasma proteins that make offending particle tasty to the phagocytes
Opsonin
Antibodies
Proteins
Enzymes
is the release of bactericidal chemical stored within granules
Degranulation
Granulation
Select the 2 oxygen dependent bactericidal mechanisms:
Respiratory burst
MPO, H202, HOCL
Lysozymes
Lactoferrin
Select the 2 oxygen independent bactericidal mechanisms:
Respiratory burst
MPO, H202, HOCL
Lysozymes
Lactoferrin
Inflammation leads to the release of numerous chemical agents that mediate the many effects of inflammation
True
False
antigen or antibody interactions
Classic pathway
Alternate pathway
C2a, C5a (Anaphylatoxins)
C5a
C3b
endotoxins, polysaccharides, globulins
Classic pathway
Alternate pathway
C2a, C5a (Anaphylatoxins)
C5a
C3b
increase vascular permeability
Classic pathway
Alternate pathway
C2a, C5a (Anaphylatoxins)
C5a
C3b
chemotactic factor
Classic pathway
Alternate pathway
C2a, C5a (Anaphylatoxins)
C5a
C3b
opsonic fragment
Classic pathway
Alternate pathway
C2a, C5a (Anaphylatoxins)
C5a
C3b
membrane attack complex
Classic pathway
Alternate pathway
C2a, C5a (Anaphylatoxins)
C5a
C5b-9
granulomas have a central areas of caseation necrosis
Tuberculosis
Leprosy
Fungal infection
Parasitic infections
numerous foamy macrophages
Tuberculosis
Leprosy
Fungal infection
Parasitic infections
schistosomiasis, granulomas around the ovum
Tuberculosis
Leprosy
Fungal infection
Parasitic infections
Thin plasma fluid or irritation of mesothelial lining cells. Blisters.
Serous inflammation
Fibrinous inflammation
Suppurative inflammation
Ulcer
Plasma proteins such as fibrin. Fibrinous pericarditis in rheumatic heart diseases.
Serous inflammation
Fibrinous inflammation
Suppurative inflammation
Ulcer
Abundant pus. Usually associated with pyogenic organisms • Example: staphylococci
Serous inflammation
Fibrinous inflammation
Suppurative inflammation
Ulcer
Excavation of the surface of an organ or tissue due to sloughing (shedding) of necrotic tissues.
Serous inflammation
Fibrinous inflammation
Suppurative inflammation
Ulcer
Replacement of injured cells by the same cell type
Regeneration
Fibrosis or Fibroplasia
Replacement of injured cells by connective tissue
Regeneration
Fibrosis or Fibroplasia
➢ Continuously dividing cells
➢ Epithelia, blood cells
Labile cells
Quiescent or Stabile cells
Permanent or Non-dividing cells
➢ Low-level of replication but can be stimulated in response to stimuli
➢ Solid visceral organs, mesenchymal tissues
Labile cells
Quiescent or Stabile cells
Permanent or Non-dividing cells
➢ Neurons, cardiac muscles, skeletal muscle
Labile cells
Quiescent or Stabile cells
Permanent or Non-dividing cells
• Healing by first intent
• Clean, uninfected wound with minimal loss of native tissues
• Deliberate surgical incisions, superficial abrasions
Primary union
Secondary union
• Healing by second intent
• More extensive injuries where there is a large tissue defect to be filled
• Major loss of native tissue
• More intense inflammation
• Larger amounts of granulation in defects
• Wound contraction
• Ulcers, avulsions, traumatic injuries
Primary union
Secondary union
Wound Healing is attributed to constant remodeling and deposition of collagen. Plateaus on the third month achieves 70 to 80 percent of original strength
True
False
Deformities of surrounding normal tissues with limitation of motion and movement
Contractures
Excessive scar
Deficient scar
• Keloid
• Hypertrophic scar
Contractures
Excessive scar
Deficient scar
