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MDTI > Inflammation > Flashcards

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
Q

2 main features of acute inflammation

A
  1. fluid exudation
  2. neutrophil emigration
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26
Q

2 main features of chronic inflammation

A
  1. scarring/fibrosis
  2. macrophages and lymphocytes
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27
Q

Vascular effects in acute inflammation

A
  1. vasodilation
  2. incrased permeability
  3. stasis
  4. leukocyte margination
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28
Q

Four key mediators that induce endothelial cell contraction in blood vessels to increase permeability

A
  1. histamine
  2. bradykinin
  3. leukotrienes
  4. VEGF
29
Q

Edema

A

accumulation of fluid extravascular compartment or interstitial tissues (stains pink)

30
Q

Exudates have a higher _______ than transudates

A

specific gravity due to protein/cell content

31
Q

Serous inflammation-morphology

A
  • watery, protein poor fluid
  • bright pink
  • few cells
32
Q

Fibrinous inflmmation-morphology

A
  • fibroblasts and vessels
  • linings of body cavities
33
Q

Suppurative inflammation-morphology

A
  • neutrophils
  • edema fluid
  • necrotic cells
  • central necrosis with scarring
34
Q

Ulcer

A

site of inflammation where epithelial surface has become necrotic and eroded/sloughed

35
Q

3 Key cellular events in inflammation

A
  1. leukocyte emigration
  2. chemotaxis
  3. leukocyte activation
36
Q

Leukocyte rolling and activation

A
  • 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
Q

Key mediator of leukocyte transmigration

A

PECAM-1/CD31

38
Q

Ways leukocytes kill ingested pathogens

A
  1. HOCL- myeloperoxidase radical
  2. bactericidal permeability increasing protein
  3. lysozyme
  4. major basic protein - parasites
39
Q

Which complement molecules are anaphylatoxins?

A

C3a and C5a

40
Q

Which complement molecule activates leukocytes via chemotaxis?

A

C5a

41
Q

Which complement molecule is an opsonin?

A

C3b

42
Q

Histamine

A
  • found in mast, basophils, platelets
  • released by truama, heat, IgE, C3a, C5a
  • vasodilation and venular endothelial contraction
43
Q

Roles of TNFalpha and IL1 in inflammation

A
  1. endothelial activation
  2. systemic acute phase reactions
  3. hypotension
  4. aggregation and activation of neutrophils, protease release, tissue damage
44
Q

NO

A
  • produced by macrophages and endothelial cells in inflammation
  • vasodilator, antagonizes platelets, microcidal
    *
45
Q

Neutral proteases

A
  • contained in neutrophil/monocyte lysosomal granules
  • e.g. elastase, collagenase
  • antiproteases like a-1 antitrypsin reduce tissue damage –> deficiency = emphysema
    *
46
Q

Chronic inflammation

A
  • 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
Q

Granulomatous inflammation

A
  • 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
Q

Granulation tissue

A
49
Q

Fever generation in acute inflammation

A
  • pyrogens
    • exogenous: lps
    • endogenous: IL1, TNF
50
Q

ESR

A

acute phase proteins (fibrinogen and Ig) in plasma neutralize neg. charges on RBCs–> no more repulsion –> staacking –> sinking in test tube

51
Q

A normal ESR rules out

A

inflammatory conditions.

52
Q

Wound healing

A

repair of damaged tissue by replacement and/or regeneration

53
Q

Regeneration

A

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
Q

Replacement

A

filling of wound with less specialized connective tissue

55
Q

Which tissues regenerate readily?

A

GI epithelium, epidermis, bone marrow

56
Q

Which tissues regnerate on a normally limited but inducible basis?

A

liver, kidney, vascular endothelia

57
Q

Healing by primary union

A

straight wound, well apposed edges, clean –> minimal scar

58
Q

Healing by secondary union

A

Irregular wound, unapposed edges, dirty –> significant scarring

59
Q

______ cells release PDGF, resulting in ______.

A
  • activated platelets and macrophages
  • proliferation of fibroblasts and vascular endothelial cells
60
Q

______ cells release FGF, resulting in ______.

A
  • macrophages and fibroblasts
  • angiogenesis
61
Q

______ cells release KGF, resulting in ______.

A
  • fibroblasts
  • growth of keratinocytes
62
Q

______ cells release VEGF, resulting in ______.

A
  • endothelial cells, fibroblasts, macrophages in hypoxic environment
  • endothelial cell proliferation, angiogenesis, vessel permeability
63
Q

______ cells release TGF beta, resulting in ______.

A
  • platelets, macrophages, fibroblasts, keratinocytes
  • A LOT
64
Q

Wound healing day 0

A
  • Clot
  • entry of acute inflammatory cells
  • chemokine and growth factor release
65
Q

Wound healing day 2

A

epithelialization

66
Q

Wound healing day 7

A

granulation tissue

67
Q

Wound healing day 14

A

disordered collagenization (type 3)

68
Q

Wound healing 1 year

A

organized scar-type 1 collagen

69
Q

What cell cycle inhibitor may limit full wound healing and is a key mediator of proliferative arrest in senescent cells?

A

p21

MDTI (10 decks)

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