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Y Pathology I (Dustin) > Topics A22-25 - Inflammation (Acute, Chronic, Granulomatous) > Flashcards

Topics A22-25 - Inflammation (Acute, Chronic, Granulomatous) Flashcards

1
Q

Classical symptoms of acute inflammation

A

Rubor, tumor, calor, dolor, loss of function

All occur due to increased blood content of inflamed tissue (historically this was the reason behind bloodletting)

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2
Q

Why does pain occur during inflammation?

Which part of the immune system is inflammation, innate or adaptive?

A

PGE2 sensitizes nerve endings to effects of bradykinin and other pain receptors

Immune system is part of Innate immunity

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3
Q

What are 4 major stimuli for inflammation?

A
  1. Infections
  2. Immune reaction, as in to a bee sting
  3. Tissue damage/ necrosis: from trauma, radiation, burns
  4. Foreign bodies: sutures, splinters, etc
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4
Q

What are the 3 major steps of acute inflammation (according to the lecture)

A
  1. Hyperemia: arteriole arteriole dilation + reduced venous outflow + capillary dilation. Flow of blood slows down at inflammation site, allowing for more interaction
  2. Exudation: Components of blood leak out into EC matrix due to increased capillary permeability (exudate = high protein)
  3. Cell migration: chemotaxis etc of protective and regenerative cells
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5
Q

What regulates the early phase of exudation in inflammation? What regulates the late phase?

A

Early: histamine, bradykinin, leukotrienes

Late: TNF, IL-1, IFN gamma

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6
Q

How does an inflammasome get activated? What is the effect?

A

Inflammasomes detect products of dead cells from pathogenic bacteria via extracellular ATP and uric acid.

Inflammasome includes caspase-1, which activates IL-1 beta. IL-1B is a major pro-inflammatory cytokine

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7
Q

What are the 4 steps of leukocyte recruitment?

A
  1. Margination / Rolling along vessel wall
  2. Adhesion to endothelium
  3. Migration between endothelial cells / Diapedesis
  4. Migration to interstitial tissues towards a chemotactic stimulus
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8
Q

What type of molecules mediate rolling?

What type of molecules mediate adhesion?

A

Rolling = selectins on leukocytes and endothelial cells

Adhesion = leukocyte integrins + endothelial cells CAMs (cellular adhesion molecules: VCAM-1, ICAM-1 etc)

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9
Q

Where in the vasculature does diapedesis normally occur?

A

In the systemic venules (high endothelial venules - HEV)

Also occurs in pulmonary capillaries

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10
Q

What are 4 things (either exogenous or endogenous) that can induce chemotaxis?

A
  1. Bacterial products, especially peptides with N-formyl methionine termini
  2. Cytokines, especially chemokines like IL-8
  3. Complement components: C5a especially
  4. Products of lipoxygenase pathway, especially leukotriene B4
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11
Q

Which type of leukocytes dominate in the first 6-24 hours of inflammation?
Which ones replace them afterwards?

What are some exceptions?

A

Neutrophils first, monocytes later, and lymphocytes usually even later on

However, in viral infections, lymphocytes may arrive first; and in hypersensitive reactions it may be eosinophils. Also, Pseudomonas infections have continuous neutrophils

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12
Q

What is the mechanism behind the two types of leukocyte adhesion deficiency (LAD?)

A

LAD-1: defective synthesis of beta 2 integrin (binds to ICAMs)

LAD-2: deficiency of endothelial cell selectin that normally binds neutrophils. Milder symptoms than type 1.

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13
Q

What is the first sign of leukocyte adhesion deficiency (LAD)?

A

Delayed separation from umbilical cord: neutrophils are important for cord separation.

They originally noted that babies who couldn’t get rid of their umbilical cord would get sick and die of infection at a very young age

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14
Q

What are 3 major ways that the immune system recognizes infection, but also necrotic cells and foreign substances? (one was already asked about).

A
  1. Toll-like receptors (TLR) - has receptors both on the membrane and internally. Various TLRs detect endotoxins, bacterial DNA, viruses, etc.
  2. Lectin receptors: MBL on complement etc
  3. Inflammasome: detects products of dead cells, like uric acid and extracellular ATP
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15
Q

How do neutrophils and macrophages actually cause harm with inflammation?

A

These leukocytes secrete degradative enzymes and ROS, killing microbes but also damaging normal cells - “innocent bystanders”

Attempts to reperfuse necrotic areas may cause more damage via this mechanism, including hemorrhage. This is also involved in carcinogenesis.

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16
Q

What is the source and effect of histamine in acute inflammation?

A

Source: mast cells, basophils, platelets

Effect: vasodilation, increased vascular permeability, endothelial activation

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17
Q

What is the source and effect of serotonin in acute inflammation?

A

Source: platelet granules, released during platelet aggregation

Effect: vasoconstriction

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18
Q

What is the source and effect of prostaglandins in acute inflammation?

A

Source: mast cells, leukocytes

Effect: vasodilation, pain, fever (esp PGE2)

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19
Q

What is the source and effect of leukotrienes in acute inflammation?

A

Source: mast cells, some leukocytes

Effect: increased vascular permeability, vasoconstriction, chemotaxis, leukocyte adhesion and activation.

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20
Q

Which leukotrienes cause vasoconstriction and increased vascular permeability?

Which cause chemotaxis and leukocyte adhesion?

A

Vasoconstriction and increased vascular permeability: Leukotriene C4, D4, E4

Chemotaxis and leukocyte adhesion: Leukotriene B4 (very potent neutrophil attractor, and also secreted by neutrophils and some macrophages)

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21
Q

What are 3 important categories of proteins / protein fragments that are produced by the liver and play a role in acute inflammation?

A
  1. Complement proteins: cause leukocyte activation and chemotaxis, directly kill microbes (MAC), and stimulate mast cells to cause vasodilation
  2. Kinins: cause pain, vasodilation, increased vascular permeability
  3. Coagulation factors: also play a role in activating endothelial cells and recruiting leukocytes
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22
Q

What are the major cytokines in acute inflammation?

A

TNF, IL-1, IL-6, and chemokines

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23
Q

What are the sources and some more local roles of TNF and IL-1 in acute inflammation?

A

Sources: activated macrophages, mast cells, endothelial cells, and some others. Inflammasomes make IL-1.

Roles: endothelial activation, increased leukocyte binding and recruitment, enhanced production of additional cytokines. TNF increases thrombogenicity, IL-1 activates tissue fibroblasts and stimulates production of IL-6

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24
Q

What are the effects of TNF, IL-1, and IL-6 on the brain and bone marrow?

What are the effects of IL-1 and IL-6 on the liver?
(these are “systemic protective effects”0

A

Brain: fever induction
Bone marrow: leukocyte production

Liver: acute phase proteins synthesized and released

25
Q

(from Robbins) - What are 3 systemic pathological effects during acute inflammation caused by TNF?

A
  1. TNF induces the heart to decrease output, lowering blood pressure
  2. TNF makes the endothelium more thrombogenic
  3. TNF and IL-1 make the skeletal muscle more insulin-resistant
26
Q

What are 3 possible outcomes of acute inflammation?

A
  1. Resolution: clearance of stimuli, mediators, and acute inflammatory cells
  2. Progression to chronic inflammation: injurious agent is not removed
  3. Scarring or fibrosis: susbtantial tissue destruction, tissue does not regenerate
27
Q

The 5 morphological patterns of inflammation, categorized by their exudate (just names, will elaborate after)

A
  1. Serous
  2. Fibrinous
  3. Purulent
  4. Hemorrhagic
  5. Gangrenous

“Serious gangs hem purple fibers”

28
Q

What is serous inflammation like? When is it seen?

A

Mildest form of inflammation. Edema has low protein content, derived from plasma secretions or secretions from mesothelial cells or peritoneum, pericardium, or pleura (fluid in serous cavity = “effusion”)

Seen in common cold, hay fever, exudative pleuritis, and blisters from burns.

29
Q

What is fibrinous inflammation like? What are the 2 main divisions of it?

A

Severe injuries cause greater vascular permeability, and larger molecules like fibrinogen pass through endothelial barrier (histo = eosinophilic meshwork, amorphous coagulation)

Types:

  1. Serous fibrinous: affects serous body linings (pericardium, meninges)
  2. Fibrinous mucous membrane: superficial necrosis precedes exudation process
30
Q

What are the two types of fibrinous mucous membrane inflammation?

A
  1. Croupous type: necrosis limited to mucosal epithelium, pseudomembrane is easy to remove
  2. Diptheria type: necrosis extends to submucosa, making the pseudomembrane difficult to remove
31
Q

What are two functions of fibrinous exudate?

A
  1. Promotes phagocytosis

2. Prevents inflammation from spreading (for example, can isolate perforated contents of appendicitis)

32
Q

What are two possible outcomes of fibrinous exudate?

A
  1. The debris is removed, resulting in restoration of normal tissue structure (“resolution”)
  2. The debris cannot be removed completely, and fibroblasts and blood vessels grow into it (“organization”), leading to scarring and adhesion
33
Q

Which slides/specimens were presented as examples of fibrinous inflammation?

A

Fibrous pericarditis slide, lobar pneumonia specimen and slide

34
Q

What is Dressler syndrome?

A

pericarditis that forms as a “post-myocardial infarction syndrome” - autoimmune reaction due to antigens associated with necrosis from the MI

35
Q

What are the 4 stages of lobar pneumonia?

A
  1. Congestion: vasodilation with edema (1-2 days)
  2. Red hepatization: feels like and has color of liver. RBCs are in parenchyma (day 3-4)
  3. Gray hepatization: red color disappears as histiocytes degrade RBCs and take up hemosiderin (day 5-6) [lobar pneumonia specimen is in this stage]
  4. Death or Resolution: patient either heals or dies
36
Q

What are the two main divisions of pneumonia? What is the difference?

A
  1. Lobar pneumonia: air spaces of one lobe are homogenously filled with exudate. Usually caused by S. pneumoniae (but can be H. influenzae or Klebsiella)
  2. Bronchopneumonia: Initially centers around bronchi and surrounding alveoli, can spread though. Generally a patchy distribution of inflammation that affects more than one lobe. More purulent than fibrinous (maybe only purulent? hard to find a source). Has patchy areas of consolidation.
37
Q

What is characteristic of purulent (suppurative) inflammation?

A

Collection of large amounts of purulent exudate (pus), consisting of neutrophils, necrotic cells, and edema fluid. Organisms like staphylococci are “pyogenic” - likely to create purulent inflammation.

38
Q

What is it called when pus is surrounded by a membrane?

What about when pus is inside of a natural anatomical cavity?

And when pus spreads in interstitium of organ?

A

Abscess: surrounded by membrane

Empyema: inside natural anatomical cavity (e.g. pleural empyema / “pyothorax”)

Phlegmon: pus spreads in interstitium of organ (e.g. diverticulitis)

39
Q

What is it called when pus accumulates deep under a hair follicle in a painful, swollen area?

What is it called when multiple ones are clustered together?

A

Furuncle or “boil”: purulent inflamed hair follicle

Carbuncle: many furuncles clustered together

40
Q

What type of necrosis occurs with a pulmonary abscess?

A

Anemic liquefactive necrosis

41
Q

Why does hemorrhagic inflammation occur, and what is in the exudate?

Can you give some examples when it occurs?

A

The inflammation involves microvascular injury with massive microvascular bleeding. The inflamed areas become necrotic and the exudate is filled with blood

Some examples: all the scary shit like smallpox, anthrax, viral hemorrhagic fever (ebola), also acute pancreatitis, hemorrhagic urocystitis, even infuenza

42
Q

General description of chronic inflammation:

A

Prolonged inflammation (weeks to years) in which continuous inflammation, tissue injury, and healing, often by fibrosis, occur simultaneously

43
Q

What are 3 scenarios that can cause chronic inflammation?

A
  1. Imbalance between host immune system and aggressiveness of microbe: microbe either too strong / immune system is too weak (e.g. TB, hep C)
  2. Meeting inorganic substances in the body that cannot be eliminated (foreign bodies: silica, etc)
  3. Hypersensitivity / Autoimmune diseases: body reacts against own antigens, never-ending process (SLE, RA)
44
Q

What are the two broad categories of chronic inflammation, based on histology?

A
  1. Non-specific: the vast majority of types (90-95%). Based on histological appearance, you can’t estimate the etiology
  2. Specific: histo gives you an educated guess. Particularly useful for TB (granulomatous inflamm), but can include other things
45
Q

What types of leukocytes are more characteristic for chronic inflammation?

A

Macrophages (dominant cell type), lymphocytes, and plasma cells (usually less neutrophils than acute inflammation)

46
Q

What are some major diseases of old age that are thought to be at least somewhat related to chronic inflammation?

A

Atherosclerosis, Diabetes Mellitus type 2, some forms of cancer, Neurodegenerative disorders like Alzheimers

47
Q

What are two ways that chronic inflammation relates to cancer?

A
  1. Chronic release of ROS by leukocytes causes DNA damage to the “innocent bystander” cells, potentially damaging their DNA
  2. Cytokines, growth factors, and chemokines all induce cell proliferation that can transform into cancer
48
Q

There are two kinds of macrophages (M1 and M2), and they have opposing responses. What are their effects and products/cytokines associated with them?

A

M1: Classically-activated, pro-inflammatory and microbicidal. They are activated by IFN gamma. Secrete ROS, NO, lysosomal enzymes, as well as IL-1, IL-12, and chemokines

M2: Alternatively-activated macrophages, anti-inflammatory and promote tissue repair. Activated by IL-4, IL-13. Secrete growth factors, TGF beta, IL-10.

49
Q

Which type of Th cells secrete cytokines related to macrophage induction in inflammation?

A

Th1 secrete IFN gamma, activating the classical macrophage pathway (M1)

Th2 cells secrete IL-4, IL-5, and IL-13, helping the alternative pathway of macrophage activation (M2)

(Th17 secrete IL-17 and induce chemokines that recruit neutrophils and monocytes)

50
Q

What type of infection are eosinophils most associated with?

Which antibody too?

A

Parasitic infections and allergy-inducing substances

Use IgE

51
Q

What is granulomatous inflammation?

A

Distinctive pattern of chronic inflammation characterized by activated macrophages, scattered lymphocytes forming a granuloma

52
Q

What are epitheloid cells? What are Langhans giant cells?

A

Epitheloid cells: in granuloma, epitheloid cells look like epithelium but they are actually macrophages that are packed in a small space

Giant cells are fused-together epitheloid cells / macrophages. They are multinucleated

53
Q

How does a granuloma appear macroscopically? What are some diseases that cause them?

A

Pale, white nodule with or without central caseation, enclosed in distinct inflammatory border.

TB is the classic reason, and some other infections like syphilis, leprosy, cat-scratch fever and whatever virus causes subacute thyroiditis can also cause granulomas.

Non-infectious forms can be from sarcoidosis or Crohn’s disease

54
Q

What are special granulomas in the myocardium called, especially after rheumatic fever?

A

Aschoff bodies or nodules

55
Q

What is sarcoidosis?

A

Chronic inflammatory disease of unknown origin that causes non-caseating granulomas throughout the body.

Most characterized by bilateral hilar lymph
adenomegaly (BHL). Often misdiagnosed as lymphoma.

End stage is called “honeycomb lung”

56
Q

What are two things to look for in the sarcoidosis histology slide?

A
  1. Asteroid bodies: look kind of like a sea anemone in the cytoplasm of giant cells
  2. Shaumann bodies: calcium deposits inside granuloma giant cells. Concentric, roundish thing. not diagnostic but suspicious for sarcoidosis
57
Q

Where does TB usually settle? Why does a granuloma form around the infection?

A

Mycobacterium tuberculosis likes air and so it deposits in subpleura, usually at inferior border of the upper lobe.

Body tries to kill them with macrophages, but bacterial waxy coat protects them and so we isolate the infection by building a granuloma around them - “immunological prison”

58
Q

Not going to make cards on the phases of tuberculosis, just a reminder to look over it and Ranke-Ghon complex

A

OK

Y Pathology I (Dustin) (20 decks)

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