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FPP: pre-midterm > Acute and Chronic Inflammation > Flashcards

Acute and Chronic Inflammation Flashcards

1
Q

What are the two functions of inflammation?

A

Destroy/contain the harmful agent and prepare for the occurence of healing/repair

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2
Q

What are the four cardinal signs of inflammation?

A

Heat, redness, swelling, pain (and loss of function)

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3
Q

What are the features of acute inflammation?

A
  • fast onset (min-hr)
  • mainly neutrophil infiltrate
  • usually mild/self-limiting tissue injury
  • prominent local and systemic signs
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4
Q

What are the features of chronic inflammation?

A
  • slow onset (days)
  • monocyte/macrophage and lymphocyte infiltrate
  • often severe/progressive tissue injury
  • less prominent local and systemic signs

**chronic inflammation may follow acute or arise de novo

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5
Q

What are the common causes of inflammation?

A
  • Infections/microbial toxins (bacteria, viruses, fungi, parasites)
  • Tissue necrosis (ischemia, trauma, etc)
  • Foreign bodies (splinters, sutures, etc)
  • Immune/hypersensitvity reactions
    • environmental substances
    • self antigens
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6
Q

What 3 ways are abnormal stimuli recognized by the body?

A
  1. Cells with receptors to detect infectious pathogens (epithelial, DCs, phagocytes, TLRs)
  2. Cell receptors that recognize molecular structures present with cell damage (e.g. inflammasomes recognize parts of dead cells in cytoplasm such as uric acid/DNA/ATP and activate caspase-1/IL-1 to recruit leukocytes)
  3. Circulating proteins (i.e. complement)
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7
Q

What are the three components of acute inflammation?

A
  1. Small vessel dilation (induced by histamine and nitric oxide… affects arterioles then capillary beds)
  2. Increased permeability of small vessels (induced by histamine and bradykinin… affects mainly venules)
  3. Margination/emigration of leukocytes from circulation, leukocyte activation
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8
Q

What causes the erythema and warmth associated with inflammation?

A

Stasis of blood flow/congestion due to the vasodilation of small vessels

**Think wider river= slow flowing, fast little stream

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9
Q

Define exudate

A

Inflammatory extravascular fluid with high protein content that may contain some white and red cells

*High specific gravity >1.020

**More serious inflammation process than the leakage of transudate, caused by alteration in normal vessel permeability

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10
Q

Define transudate

A

Non-inflammatory extravascular fluid with low protein content and few cells (ultrafiltrate of plasma)

*Low specific gravity <1.012

**Leakage due to increased hydrostatic pressure/decreased colloid osmotic pressure… more mild than exudate leakage

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11
Q

Define pus

A

Purulent thick exudate rich in leukocytes

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12
Q

Define edema

A

Excess fluid in interstitium or serosal cavities

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13
Q

Describe how histamine is released and its effect on vessels

A
  • Released from mast cells in connective tissue in response to cytokines (IL1), trauma, complement, etc
  • Causes vasodilation and increased vascular permeability
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14
Q

Describe how nitric oxide is released and its effect on vessels

A
  • Many functions/origins
  • In inflammation; released by endothelial cells in response to injury and causes vasodilation
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15
Q

Describe what bradykinin is and its effect on vessels

A
  • Plasma protein resulting from kinin system activation (exposure to site of endothelial injury)
  • Causes vasodilation, increased permeability, and pain
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16
Q

What is the origin of neutrophils? macrophages?

A

Neutrophils are from hematopoietic stem cells in marrow

Macrophages are from hematopoietic stem cells in marrow in inflammatory reactions AND many tissue-resident macrophages come from stem cells in development

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17
Q

What is the life span of neutrophils? macrophages?

A

Neutrophils= 1-2 days (short)

Inflammatory Macrophages= days-weeks (long)

Tissue-resident Macrophages= years (long)

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18
Q

What is the response of neutrophils to stimuli? of macrophages?

A

Neutrophils= rapid, short-lived response

Macrophages= more prolonged, slower, dependent on new gene transcription

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19
Q

Define leukocyte margination

A

Movement closer to vessel wall (due to vasodilation and stasis)

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20
Q

What are the two main adhesion molecules that help with rolling/adhesion of leukocytes to the endothelial cells?

A

Selectins (on endothelial cells, platelets, leukocytes); not present until cell activation by mediators (histamine, thrombin, etc)… aid in rolling and loose attachment

Integrins (on leukocytes) activated by chemokines on endothelial cells… results in stable attachment

21
Q

Define diapedesis

A

Movement of leukocytes through vessel walls (cells squeeze through endothelial cells, driven by chemokine CD31/PECAM1 on leukocytes and endothelial cells)

22
Q

Define chemotaxis

A

Movement along a chemical gradient (after crossing vessel wall, cells migrate towards injury site via gradients of chemokines/complement/leukotrienes)

23
Q

What are the results of leukocyte activation?

A
  1. phagocytosis
  2. intracellular destruction
  3. release of substances that destroy dead tissue and microbes
  4. more mediator production (amplify inflammatory reaction)
24
Q

What substances act to activate leukocytes?

A

Microbes, necrotic tissue, mediators (activate leukocytes after recruitment to the site of injury)

25
Q

What two ways can leukocytes recognize a microbe?

A
  1. Specific surface receptors for microbe on the leukocyte
  2. Receptors for opsonins (IgG, complement, lectins)
26
Q

What two mediators induce vasodilation? Where do they come from?

A
  1. Histamine (from mast cells, basophils, platelets)
  2. Nitric oxide (from endothelium and macrophages)
27
Q

What two mediators increase vascular permeablity? Where do they come from?

A
  1. Histamine (from mast cells, basophils, platelets)
  2. Bradykinin (from plasma; produced in liver)
28
Q

What two mediators induce chemotaxis/recruitment/activation of leukocytes? Where do they come from?

A
  1. IL1/TNF (from macrophages, endothelial cells and mast cells)
  2. Bacterial products (from bacteria lol duh)
29
Q

What two mediators induce fever? Where do they come from?

A

IL1/TNF (both from macrophages, endothelial cells, and mast cells)

30
Q

What mediator induces pain? Where does it come from?

A

Bradykinin from mast cells, leukocyted, and plasma (produced in the liver)

31
Q

What two mediators induce tissue damage? Where do they come from?

A
  1. ROS (from leukocytes)
  2. Nitric oxide (from endothelium and macrophages)
32
Q

What are some common defects in leukocyte inflammation function?

A
  1. Production defect (BM suppression from chemo/radiation)
  2. Adhesion/chemotaxis defect (spesis, diabetes, dialysis, malignancy)
  3. Phagocytosis and microbicidal activity defect (sepsis, diabetes, anemia, malnutrition)

**Genetic defects are RARE

33
Q

What are the general characteristics of all acute inflammation?

A
  1. Accumulation of leukocytes (neutrophils and macrophages) **NOT lymphocytes!
  2. Fluid build up in extracellular tissue
  3. Dilation of small blood vessels
34
Q

What are the subtypes of acute inflammation?

A
  1. Serous
  2. Fibrinous
  3. Suppurative/purulent
35
Q

Describe serous inflammation

A

Most mild type of acute inflammation; outpouring of transudate
E.g. Effusions or blisters

36
Q

Describe fibrinous inflammation

A

“in between” acute inflammation severity, fibrinogen leakage converts to fibrin -> scarring

**Affects linings (meninges, pericardium, pleura, etc)
E.g. Pericarditis, pleuritis, peritonitis

37
Q

Describe suppurative inflammation

A

Most severe acute inflammation, large # of neutrophils with necrotic cells, edema fluid and bacteria -> PUS

**More likely with pyogenic (e.g. staph) bacteria
E.g. Acute appendicitis, bronchopneumonia, meningitis

38
Q

Define ulcer

A

Local defect on the surface of an organ/tissue characterized by sloughing of surface and necrotic inflammatory tissue

E.g. peptic ulcer, skin ulcer (esp with diabetes)

39
Q

Define chronic inflammation

A

Active inflammation, tissue injury, and healing occuring at the same time for months to years

40
Q

What are the common causes of chronic inflammation?

A
  1. Persistent infections (e.g. TB, syphilis, chronic lung abscess)
  2. Prolonged exposure to toxic agents (exogenous e.g. silicosis, or endogenous e.g. atherosclerosis)
  3. Hypersensitivity diseases (autoimmune or allergy)
41
Q

What characterizes chronic inflammation?

A
  1. Infiltration by mononuclear cells (macrophages, lymphocytes, plasma cells)
  2. Tissue destruction (by persistent injurious agent and/or inflammatory cells)
  3. Attempts at healing (angiogenesis and fibrosis)
42
Q

What are the two types of granuloma?

A
  1. Immune (from persisten microbe or self-antigen)
    E.g. TB, syphilis, Crohn’s, autoimmune
  2. Foreign body (from inert foreign bodies without a T cell mediated immune response)
    E.g. sutures, splinters
43
Q

Describe granulomatous inflammation

A
  • Aggregates of epithelioid histiocytes (macrophages)
  • Multinucleated giant cells= fusion of many macrophages (induced by IFN gamma)
  • Collar of lymphocytes/plasma cells with surrounding fibrosis

**Seen in TB and with foreign bodies/other infections

44
Q

What are the systemic effects of inflammation?

A

Called “acute phase response”:

  • reaction to cytokines (TNF, IL1, IL6)
  • fever
  • elevated plasma levels of acute-phase proteins
  • leukocytosis
45
Q

What causes fever in the inflammatory response?

A

Pyrogens (exogenous such as bacterial endotoxins or endogenous such as IL1/TNF from leukocytes)

**Pyrogens cause production of PGE2 (which stimulates hypothalamus to reset at a higher temp)

46
Q

What are some examples of acute-phase proteins? What are their actions?

A

**synthesized in liver, stimulated by IL6;

  1. C-reactive protein (CRP)
  2. Fibrinogen
  3. Serum amyloid A protein (SAA)

**Actions:

  • bind microbe wall (aid in elimination)
  • fibrinogen binds erythrocytes, causing stacks (rouleaux) that sediment more rapidly than normal resulting in:
    • elevation of erythrocyte sedimentation rate (ESR)
    • increased sed rate in ingections/autoimmune inflammatory disorders
47
Q

What stimulates leukocytosis? What is the WBC count that defines leukocytosis?

A

Stimulated by TNF and IL1

WBC count usually high (between 15,000-20,000 cells/mL) because of accelerated release of cells from BM

48
Q

What are the four main types of leukocytosis and what underlying cause do they reflect?

A
  1. Neutrophilia- bacterial infection (“left shift”/accelerate release of immature neutrophils)
  2. Lymphocytosis- viral infection
  3. Eosinophilia- allergies, asthma, parasitic infection
  4. Leukopenia- typhoid, rickettsiae, some protozoans

FPP: pre-midterm (19 decks)

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