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High Yield > PATH > Flashcards

PATH Flashcards

1
Q

What mediates transmigration in acute inflammation?

A

PECAM-1 on endothelial cells and CD31 on leukocytes (homotypic like like interactions)

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2
Q

What does activation of toll like receptors lead to?

A

Up regulation of NF-kB

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3
Q

How is the acute inflammatory response terminated?

A

Mediators only produced transiently
- and regulated by stop signals such as:

Switch of leukotrienes to lipoxins (anti-inflammatory form)

Production of anti-inflammatory cytokines such as TFG-B and IL-10

Neural impulses that inhibit macrophage TNF production

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4
Q

Examples of chemical mediators of inflammation?

A 
Vasoactive amine
Plasma proteases
Phospholipid derived products
Cytokines
Nitric oxide
Lysosomal enzymes
oxygen derived free radicals
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5
Q

Beneficial effects of inflammation?

A 
Dilution of toxins
Arrival of antibodies to site of inflammation
Drug transport
Delivery of nutrients and oxygen
Fibrinogen converted to fibrin
Destruction of microbial agent
Removal of tissue debris
Stimulation of immune response
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6
Q

Pyrogens stimulate which cells to release what?

A

Macrophages to release IL-1 and TNF

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7
Q

What is platelet activating factor?

A

Increases vascular permeability

Lipid mediator that allows aggregation of platelets and mediator of leucocyte functions

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8
Q

Harmful effects on inflammation?

A

Mechanical effect such as epiglottitis
Impaired flow e.g. acute meningitis
Impaired function
Tissue destruction

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9
Q

Outcomes of inflammation?

A
  1. Resolution
    Complete resolution with regeneration of native cells
  2. Healing and repair
    Healing by connective tissue replacement (fibrosis) occurs:
    - after substantial tissue destruction
    - setting of abundant fibrin exudation (organization)
  3. Progression to chronic inflammation
    - where injurious agents cant effectively be eliminated
  4. Abscess formation
    Abscess is a walled off collection of pus
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10
Q

Morphological features of inflammation?

A

Infiltration with mononuclear inflammatory cells such as macrophages, lymphocytes and plasma cells.
As well as tissue destruction due to persistent injury or inflammation.
Repair granulation tissue due to angiogenesis and fibrosis.

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11
Q

What activates macrophages to become larger?

A

Cytokines and bacterial endotoxins

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12
Q

How do macrophages evolve from type M1 to M2?

A

By IL13 and IL-4

Convert to M2 for wound repair

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13
Q

What are substances released by macrophages that cause tissue destruction?

A 
Proteases and other enzymes
Aa metabolites
Toxic oxygen metabolites
NO
Coagulation factors
Neutrophil chemotactic factors
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14
Q

What are substances released by macrophages that cause vascular proliferation?

A

Growth factors
Cytokines
Remodeling collagenases and metalloproteinases

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15
Q

What induces formation of classical macrophages, M1?

A

Microbial products

IFN-g

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16
Q

Causes of granulomatous inflammation?

A 
Infection (specific types)
Foreign body
Response to tumors
Metal/dust (silicosis/berylliosis)
Unknown etiology (sarcoidosis/ crohns disease)
17
Q

When does a foreign body granuloma occur? Types?

A

It occurs in response to poorly digestible foreign material,

  • exogenous such as splinter, suture, graft material
  • endogenous due to keratin or pilonidal sinus
18
Q

Examples of type four delayed hypersensitivity

A

Langerhaans giant cells

TB caseous necrosis

19
Q

What distinguishes ulcers from erosions?

A

Extent of tissue loss

20
Q

What is a sinus?

Examples?

A

A tract lined by granulation tissue leading from a chronically inflamed cavity to a surface.
Examples include:
- sinuses associated with osteomyelitis (inflammation of bone)
- pilonidal sinus (nest of hairs)

21
Q

Mechanisms associated with cell injury?

A

Inhibition of aerobic respiration causes ATP depletion
Generation of oxygen species (free radicals)
Defects in membrane permeability
Disruption of calcium homeostasis (calcium influx)

22
Q

Describe reversible injury

A

Increased anaerobic glycolysis
Reduced activity of sodium pump causing accumulation of sodium and water.
Reduced activity of calcium pump increases cytosolic free calcium and activates enzymes:

  • ATPase causing decreased ATP
  • phospholipase decreasing phospholipids
  • endonuclease causing nuclear chromatin damage
  • protease causing disruption of membrane and cytoskeletal proteins
23
Q

What are factors that affect the healing process?

A 
Ability to remove the causative agent
Ability to clear the inflammatory debris
Degree of architectural damage
Ability of cell to proliferate
Extent of damage to ECM
24
Q

What are polypeptide growth factors?

A

They are the most important mediators affwcting cell growth:

  • present in serum or produced locally
  • exert pleiotropic effects such as proliferation, cell migration, differentiation and tissue remodeling
  • regulate growth of cells by controlling expression of genes that regulate cell proliferation
25
Q

What does extracellular matrix consist of?

A

Interstitial matrix

Basement membrane

26
Q

When does healing by fibrosis occur?

A

Destruction to both parenchyma, and stromal tissues
Death to permanent cells
Organization of inflammation

27
Q

Repair by connective tissue involves?

A

Production of granulation tissue

28
Q

Local factors that influence healing

A 
Poor vascular supply
Infection
Foreign material
Excessive movement
Poor approximation
Size, site and type of injury
29
Q

Systemic factors that influence healing

A 
Age
Nutrition (proteins,  vitamin C, copper, zinc)
Metabolic status
Hormones (steroids)
Malignancy
Chemotherapy
Radiotherapy
30
Q

Two main parts to amyloid, and their pathologic function?

A

Circulating oligomers which are cytotoxic

Fibrils cause distortion of the tissue architecture

Both lead to organ dysfunction

31
Q

Nonfibrillar pentagonal glycoprotein known as ?

A

Amyloid P component

Derived from serum amyloid P

32
Q

Clinopathic category where A beta 2 microglobulin presents?

A

Hemodialysis associated amyloidosis

33
Q

Where is ATTR seen?

A

Familial amyloidotic neuropathies

Systemic senile amyloidosis

High Yield (2 decks)

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