General Pathological Mechanisms Flashcards

1
Q

What are the three types of cell found in our body?

A

1) Labile - Good capacity to proliferate e.g. skin and intestine
2) Stable - Divide at a slow rate but are still able to divide when necessary e.g. hepatocytes
3) Permanent - No effective capacity to divide e.g. neurones

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2
Q

What are the most common stains used in cellular pathology?

A
Schiff Stain - Fungi
Gram Stain - Bacteria 
Perts Stain - Iron 
Reticulin Stain - Collagen 
Congo Red Stain - Amyloid
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3
Q

Describe the process through which tissue injury leads to the release of cytokines

A

1) Epithelial barrier is breached
2) Toll Like Receptors on the epithelial cells surface recognises the pathogen associated molecular pattern (PAMP)
3) The activated TLRs release cytokines to bring WBCs to the area

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4
Q

Describe the stages of leukocyte extravasation

A

1) Leukocytosis - Neutrophils enter the blood stream via the bone marrow
2) Margination - Neutrophils cling to the surface of the capillary wall and roll along it (accelerated by selectins)
3) Diapedesis - Neutrophils flatten and squeeze out of capillaries
4) Chemotaxis - Neutrophils follow a chemical trail to the site of infection (accelerated by integrins)

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5
Q

Describe the three ways complement can be activated

A
  • Classical pathway - Antigen-antibody complex
  • MB-Lectin-Pathway - Circulating proteins known as Mannose-Binding Lectin, bind to Mannose groups on the pathogen’s surface
  • Alternative Pathway - Complement spontaneously interacts with the surface of pathogens
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6
Q

Describe the three functions of complement

A
  • Opsonisation - Makes phagocytosis of pathogen easier by coating them
  • Chemotaxis - Recruit inflammatory cells
  • Cell Lysis - Complement proteins come together to form a ‘Membrane Attack Complex’ which forms a pore in the cell
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7
Q

Describe the presentation of intracellular antigens

A

1) Endogenous antigen is degraded by proteases into peptides
2) Peptides enter ER via transport proteins
3) Peptides are loaded onto the Class I MHC protein
4) MHC protein is loaded into a vesicle and migrates to the plasma membrane

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8
Q

Describe the presentation of extracellular antigens

A

1) The extracellular antigen is phagocytised and ingested as a phagosome
2) A Class II MHC protein is synthesised at the ER and transported to the phagosome
3) The phagosome merges with the lysosome to form a phagolysosome
4) The antigen is broken down
5) The Class II MHC protein is loaded with the antigen and migrates to the plasma membrane

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9
Q

Describe the activation of the humoral immune response

A

1) B Cell becomes an APC by presenting the antigen on a Class II MHC protein
2) Activated Th cells bind with the MHC protein and release cytokines
3) Cytokines activate the B cell
a) The B cells divide to become B memory cells
b) Differentiate into plasma cells to produce antibodies

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10
Q

What are the five types of hypersensitivity reaction?

A
  • Type I - Immediate (atopic) e.g. asthma
  • Type II - Cytotoxic (antibody dependent) e.g. Bullous Pemphigoid
  • Type III - Immune Complex e.g. Lupus
  • Type IV - Delayed hypersensitivity (cell-mediated) e.g. Nickel allergy
  • Type V - Receptor mediated (subtype of type II)
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11
Q

What are the stages of a type I hypersensitivity reaction?

A

1) Sensitisation
2) Mast cell priming
3) Re-exposure to antigen
4) De-granulation of mast cell
5) Increased severity

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12
Q

Describe the early and late phase responses to mast cell de-granulation

A

Early - Minutes after exposure
- Smooth muscle contraction
- Increased vascular permeability
Late - Hours to days after exposure
- Recruitment of T cells
- Sustained smooth muscle contraction/hypertrophy
- Tissue remodelling

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13
Q

Describe the stages of a type II hypersensitivity reaction

A

1) Sensitisation
2) Opsonisation
3) Cytotoxicity

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14
Q

Describe the stages of a type IV hypersensitivity reaction

A

1) Penetration
2) Presentation
3) Reaction
4) Inflammation

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15
Q

Describe Virchow’s traid

A

Three factors required for thrombosis;

1) BLOOD COMPOSITION (hypercoagulable state)
2) BLOOD FLOW (circulatory stasis)
3) VESSEL WALL (vessel wall injury)

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16
Q

What are the four possible outcomes of acute inflammation?

A

1) Resolution - Complete restoration of tissue to normal
2) Suppuration - Formation of pus and possibly an abscess
3) Organisation - Tissue is replaced with granulation tissue
4) Chronic inflammation

17
Q

What are the two types of activated macrophages?

A

M1 (Inflammatory) Macrophage - Destroys pathogens but in doing so causes tissue injury. They secret cytokines that have a positive feedback on TH1 cells

M2 Macrophage - Facilitates wound repair and fibrosis. They secrete cytokines that have a negative feedback on TH2 cells

18
Q

What is granulomatous inflammation?

A

Chronic inflammation with two main cell types;

  • Epithelioid macrophages
  • Giant cells (fused epithelioid macrophages)
19
Q

What are the two phases of healing?

A

1) Regeneration - Specialised cells are able to grow back and the same type of cells are replaced
2) Repair - A connective tissue response when lost tissue is replaced by granulation tissue that becomes fibrous tissue

20
Q

Describe the process of tissue repair

A

1) Platelets and fibrin form a clot
2) Debris is removed by the influx of macrophages
3) Proliferation of fibroblasts and the ingrowth of new blood vessels (angiogenesis)
4) Increased collagen production provides tensile strength
5) Over time vascularity decreases and fibrous scar tissue is formed