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MS2 Block 1 > Pathology > Flashcards

Pathology Flashcards

1
Q

5 Cardinal Signs of Acute Inflammation

A
  1. Rubor
  2. Calor
  3. Tumor
  4. Dolor
  5. Functio Laesa

*1, 2, &3 due to vascular changes (Relaxation of smooth muscle of arterioles and precapillary sphincters

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2
Q

Transudate Characteristics (3)

A
  1. Ultrafiltrate of serum
  2. Specific gravity < 1.012
  3. Typically transparent
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3
Q

Exudate Characteristics (3)

A
  1. Protein Rich (albumin, fibrinogen, immunoglobulin)
  2. Specific gravity > 1.02
  3. Can be cloudy in appearance
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4
Q

Jobs of the Lymphatic System (3)

A
  1. Remove fluid exudate leukocytes, cell debris, plasma proteins, and fibrin
  2. Conduit for dendritic cells delivering antigens to lymph nodes
  3. Carry inflammatory mediators away from site, modulating the inflammatory response
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5
Q

Vasoactive Amines (2)

A
  1. Histamine
  2. Serotonin (5-HT)
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6
Q

Histamine is released following: (3)

A
  1. Trauma or exposure to heat or other injurious stimuli
  2. Binding of IgE to Fc receptors on mast cells in hypersensitivity reactions
  3. C3a and C5a fragments of complement induce mast cell degranulation
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7
Q

Plasma Proteases (Inflammatory)

A
  1. The Kinin System
  2. The Fibrinolytic System
  3. Complement
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8
Q

What does the Kinin system do?

A
  • Ultimately produces Bradykinin, a vasoactive peptide that inc vascular perm and cause vasodilation (Intrinsic Pathway)
  • Hageman Factor XII binds to neg charged substance or collagen in damaged tissue
  • Bradykinin also induces pain and contraction of non-vascular smooth muscle of airways (bronchoconstriction)
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9
Q

What does the Fibrinolytic System do?

A
  • Factor XII initiates a cascade that generates Plasmin
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10
Q

What does Plasmin do? (3)

A
  1. Digest fibrin in the clot to form Fibrin split products –> inc vasc. perm.
  2. Cleaves kininogens to form Bradykinin
  3. Activates Complement by cleaving C3
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11
Q

Complement System role in Acute Inflammation (4)

A
  1. Mediate vasc. resp. via Histamine
  2. Chemotaxis of Neutrophils
  3. Opsonization
  4. MAC: direct damage to target cells
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12
Q

Role of Complement protiens: C3a, C3b, C5a, C5b-C9

A
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13
Q

Proteins involved in “Rolling” stage of Neutrophil Margination

A
  1. P/E Selectin on EC’s
  2. L Selectin on Neutros
  3. Sialylated oligosaccharides on cell surfaces (Sialyl-Lewis X)
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14
Q

Proteins involved in Neutrophil “Adhesion”

A
  • Integrins on Neutros
  • ICAM-1/VCAM ligands on EC’s (induced by IL-1 and TNF
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15
Q

Chemotactic factors for diapedesis

A
  1. Bacterial products
  2. C5a
  3. Chemokines
  4. LTB4
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16
Q

ROS pathway

A
  • O2 to Superoxide via NADPH Oxidase
  • O2•- to H2O2 via Superoxide Dismutase (SOD)
  • H2O2 to HOCL• (Hypochlorite) via Myeloperoxidase (MPO)
17
Q

4 Rare diseases caused by Neutrophil dysfunction

A
  1. Leukocyte adhesion deficiency type I (LAD-1): defective synth. of CD18-ß subunit of leukocyte Integrins (*Affects Adhesion)
  2. LAD-2: defect in fucose metabolism –> absence of Sialyl-Lewis X –> no Selectin binding (*Affects Rolling, and some Adhesion)
  3. Defects in Microbicidal Activity: ROS
  4. Defects in Phogolysosome formation: Chediak-Higashi syndrome (affects secretory efforts of cytotoxic lymphocytes; Albinism common)
18
Q

Outcomes of Acute Inflammation (3)

A
  1. Complete Resolution
  2. Progression to Chronic Inflammation
  3. Scarring or Fibrosis
19
Q

Patterns of Acute Inflammation (4)

A
  1. Serous Inflammation (Transudate, body cavities/blisters)
  2. Fibrinous Inflammation (Exudate, Adhesions/Scars)
  3. Suppurative Inflammation (Abscess)
  4. Ulcer (Granulation tissue formed)
20
Q

Causes of Chronic Inflammation

A
  1. Infectious Agents
  2. Foreign Bodies
  3. Products of Metabolism
  4. Immune Reactions
21
Q

An adjective describing chronic inflammation that contains activated ofr epithelioid macrophages or giant cells

A

Granulomatous

*Granulomatous Inflammatory response may not contain granulomas

22
Q

These are found in the context of granulomatous inflammation; they are compact, centrally organized collections of macrophags and epithelioid cells and often giant cells

A

Granulomas

23
Q

Tissue you find under a scab; consists of loose conn. tissue and new blood vessels growing into the fibrin over the wound

A

Granulation Tissue

24
Q

2 pathways for Macrophage activation

A
  1. Classical (M1): stimulation by LPS, IFN-gamma from lymphocytes, presence of foreign bodies; Macrophages from this pathway are adept at killing via lysosomal enzymes, ROS, and NO
  2. Alternative (M2): stimulation w/ IL-4 and IL-13; macrophages from this pathway important in healing process, secret growth factors for angiogenesis and fibroplasia
25
Q

Acute Phase Clinical Tests (2)

A
  1. ESR: to detect systemic Inflammatory response
  2. C-Reactive Protein: to monitor low-grade inflammatory disease
26
Q

Important contributions that Fever adds to the healing process (4)

A
  1. Inc. mobility of leukocytes
  2. Enhanced Phagocytosis
  3. Inc. proliferation of T-Cells
  4. Compromise survival of temp sensitive pathogens

MS2 Block 1 (9 decks)

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