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Inflammation Flashcards

1
Q

2 key mechanisms of cellular injury

A
  • hypoxia
  • ischemia
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2
Q

4 cellular adaptations to injury

A
  1. hyperplasia
  2. hypertrophy
  3. atrophy
  4. metaplasia
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3
Q

hyperplasia

A
  • increase in # of cells in organ or tissue
  • often related to increase in demand for fxn
  • may be associated with increase in cell size
    • normal- uterus
    • compensatory - liver repair
    • pathalogic-graves
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4
Q

Autoimmune antibodies associated with Graves

A

HLAB8, HLADR3

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5
Q

Graves Pathogenesis

A

ab bind to TSH receptor –> increase TH hormone –> hyperplasia –> hyperthyroidism

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6
Q

Hypertrophy

A
  • increase in cell size due to increased protein synthesis (not cell swelling)
  • increased demand for function
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7
Q

Atrophy

A
  • decrease in cell size
  • decreased workload, decreased blood supply, inadequate nutrition, loss of endocrin, denervation
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8
Q

Spinal Muscular Atrophy (SMA) Pathogenesis

A

mutation in SMN1 gene –> LOF –>neuronal death –> atrophy of muscle

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9
Q

Metaplasia

A
  • reversible change in differentiation program of tissue stem cells to different cell type
  • e.g. columnar to squamous metaplasia of respiratory tract in response to cigarettes
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10
Q

Why is ischemia more rapidly injurious than hypoxia?

A

loss of both oxygen and nutrients

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11
Q

Factors of irreversible cell injur

A
  • severe mitochondrial swelling –> free radical production and release
  • extensive membrane damage –> Ca influx –> enzyme activation –> digestion of cell
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12
Q

Anti-oxidant mediators

A
  1. superoxide dismutase
  2. catalase
  3. glutathione peroxidase
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13
Q

Free radical effects on cell

A
  1. DNA –> breaks, modifications
  2. proteins –> misfolding, cross-linking
  3. lipid peroxidation –> unstable, chain-reactive
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14
Q

CCL4 mediated cellular injury - MOA

A

CCL4 –> converted to CCL3 radical by P450 –> lipid peroxidation –> diminished protein synthesis in ER –> reduced export from ER –> fat retention –> autocatalyzed peroxidation –> Ca influx –> death

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15
Q

Necrosis

A

morphologic changes due to degradative actions of enzymes on lethally inured cell

  1. coagulative
  2. liquefactive
  3. caseous
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16
Q

Coagulative necrosis-features

A
  • acidophilic (pink) cytoplasm
  • nuclei disappearance
  • preservation of cell architecture
  • hyperemic border
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17
Q

Coagulative necrosis is indicative of what process?

A

Irreversible ischemic injury

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18
Q

Liquefactive necrosis-features

A
  • hydrolytic enzymes predominate
  • rapid softening
  • loss of architecture
  • abscess formation
  • brain and pus
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19
Q

Abscess

A

focal localized collection of bacteria and pus with fibrotic border w/liquefactive necrosis

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20
Q

Caseous necrosis-features

A
  • incomplete liquefication of celular architecture
  • cheesy
  • granulomatous inflammatory wall
  • mycobacteria
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21
Q

Apoptosis

A

regulated programmed cell death to eliminate unwanted cells

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22
Q

Apoptosis-features

A
  • cells shrink
  • chromatin condenses
  • blebs form
  • phagocytosis
  • plasma membrane remains intact
  • no inflammation
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23
Q

Apoptosis triggers

A
  1. withdrawal of growth factors
  2. receptor-ligand interactions (FAS)
  3. CTL mediated
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24
Q
A
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25
2 main features of acute inflammation
1. fluid exudation 2. neutrophil emigration
26
2 main features of chronic inflammation
1. scarring/fibrosis 2. macrophages and lymphocytes
27
Vascular effects in acute inflammation
1. vasodilation 2. incrased permeability 3. stasis 4. leukocyte margination
28
Four key mediators that induce endothelial cell contraction in blood vessels to increase permeability
1. histamine 2. bradykinin 3. leukotrienes 4. VEGF
29
Edema
accumulation of fluid extravascular compartment or interstitial tissues (stains pink)
30
Exudates have a higher _______ than transudates
specific gravity due to protein/cell content
31
Serous inflammation-morphology
* watery, protein poor fluid * bright pink * few cells
32
Fibrinous inflmmation-morphology
* fibroblasts and vessels * linings of body cavities
33
Suppurative inflammation-morphology
* neutrophils * edema fluid * necrotic cells * central necrosis with scarring
34
Ulcer
site of inflammation where epithelial surface has become necrotic and eroded/sloughed
35
3 Key cellular events in inflammation
1. leukocyte emigration 2. chemotaxis 3. leukocyte activation
36
Leukocyte rolling and activation
* rolling mediated by selectins --\> bind w/low affinity to leukocytes * integrins finally bind strongly * leukocytes spread out on endothelial surface * trnasmigration via PECAM-1/CD31
37
Key mediator of leukocyte transmigration
PECAM-1/CD31
38
Ways leukocytes kill ingested pathogens
1. HOCL- myeloperoxidase radical 2. bactericidal permeability increasing protein 3. lysozyme 4. major basic protein - parasites
39
Which complement molecules are anaphylatoxins?
C3a and C5a
40
Which complement molecule activates leukocytes via chemotaxis?
C5a
41
Which complement molecule is an opsonin?
C3b
42
Histamine
* found in mast, basophils, platelets * released by truama, heat, IgE, C3a, C5a * vasodilation and venular endothelial contraction
43
Roles of TNFalpha and IL1 in inflammation
1. endothelial activation 2. systemic acute phase reactions 3. hypotension 4. aggregation and activation of neutrophils, protease release, tissue damage
44
NO
* produced by macrophages and endothelial cells in inflammation * vasodilator, antagonizes platelets, microcidal *
45
Neutral proteases
* contained in neutrophil/monocyte lysosomal granules * e.g. elastase, collagenase * antiproteases like a-1 antitrypsin reduce tissue damage --\> deficiency = emphysema *
46
Chronic inflammation
* can coexist with acute * can be caused by acute or start off chronic * accumulation of APCs (macrophages, lymphocytes, plasma cells) --\> lymphocytic infiltrate * angiogenesis and feibrosis
47
Granulomatous inflammation
* characterized by epithelioid histiocyte cells -activated macrophages that are squamous (abundant pink cytoplasm) * multinucleated giant cells (langhans) * wall off injury 1. tb 2. leprosy 3. syphilis 4. cat scratch 5. parasitic 6. fungal 7. silicosis 8. foreign bodies (sutures 9. sarcoidosis 10. crohn's
48
Granulation tissue
49
Fever generation in acute inflammation
* pyrogens * exogenous: lps * endogenous: IL1, TNF
50
ESR
acute phase proteins (fibrinogen and Ig) in plasma neutralize neg. charges on RBCs--\> no more repulsion --\> staacking --\> sinking in test tube
51
A normal ESR rules out
inflammatory conditions.
52
Wound healing
repair of damaged tissue by replacement and/or regeneration
53
Regeneration
restoration of lost tissue structures via cell division 1. division of parnchymal cells in normal stroma (post-CCL4 exposure) 2. compensatory division of parenchymal cells (after hepatectomy) 3. stem cell division
54
Replacement
filling of wound with less specialized connective tissue
55
Which tissues regenerate readily?
GI epithelium, epidermis, bone marrow
56
Which tissues regnerate on a normally limited but inducible basis?
liver, kidney, vascular endothelia
57
Healing by primary union
straight wound, well apposed edges, clean --\> minimal scar
58
Healing by secondary union
Irregular wound, unapposed edges, dirty --\> significant scarring
59
\_\_\_\_\_\_ cells release PDGF, resulting in \_\_\_\_\_\_.
* activated platelets and macrophages * proliferation of fibroblasts and vascular endothelial cells
60
\_\_\_\_\_\_ cells release FGF, resulting in \_\_\_\_\_\_.
* macrophages and fibroblasts * angiogenesis
61
\_\_\_\_\_\_ cells release KGF, resulting in \_\_\_\_\_\_.
* fibroblasts * growth of keratinocytes
62
\_\_\_\_\_\_ cells release VEGF, resulting in \_\_\_\_\_\_.
* endothelial cells, fibroblasts, macrophages in hypoxic environment * endothelial cell proliferation, angiogenesis, vessel permeability
63
\_\_\_\_\_\_ cells release TGF beta, resulting in \_\_\_\_\_\_.
* platelets, macrophages, fibroblasts, keratinocytes * A LOT
64
Wound healing day 0
* Clot * entry of acute inflammatory cells * chemokine and growth factor release
65
Wound healing day 2
epithelialization
66
Wound healing day 7
granulation tissue
67
Wound healing day 14
disordered collagenization (type 3)
68
Wound healing 1 year
organized scar-type 1 collagen
69
What cell cycle inhibitor may limit full wound healing and is a key mediator of proliferative arrest in senescent cells?
p21

MDTI (10 decks)

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