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Exam 2 - Inflammation/Injury Flashcards

1
Q

4 Cellular Adaptations to Stress

A

Hypertrophy
Hyperplasia
Atrophy
Metaplasia

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2
Q

Metaplasia

A 
Differentiated cellular change
New cell type better adapted to stress
Fertile ground for cancer (no inherent malignancy)
Barret esophagus (intestinal metaplasia)
Squamous metaplasia (lungs, smoking)
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3
Q

Reversible Cell Injury types and changes

A

Cellular swelling, fatty change
Intracelluar changes:
1. PM alterations
2. Mito changes (swelling, lipo densities)
3. ER dilation, detachment of ribosomes
4. Nuclear alterations, chromatin clumping

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4
Q

Irreversible cell injury types

A

Necrosis

Apoptosis

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5
Q 
Necrosis features
(Cell size, nuc changes, PM changes, contents, inflammation?)
A 
Cell swell
Pkynosis to lysis
PM disrupted
Contents leak
Inflammation
Pathologic
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6
Q 
Apoptosis features
(Cell size, nuc changes, PM changes, contents, inflammation?)
A 
Cell shrink
Nuclear fragmentation
PM intact, but altered
Contents don't leak
No inflammation
Physiologic
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7
Q

5 Patterns of necrosis

A 
Coagulative
Liquefactive
Caseous
Fat
Fibrinoid
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8
Q

Coagulative necrosis

A

Tissue structure preserved
Ghost cells
Characteristic of infarcts

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9
Q

Liquefactive necrosis

A

Inflammatory accumulation
Leukocytes digest tissue
Bacterial/fungal infections, CNS hypoxia

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10
Q

Caseous necrosis

A

White necrosis
Granulomatous inflammation
Necrotizing granuloma
Acid fast bacilli stain

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11
Q

Fat necrosis

A

Break down of fat by lipases
Metabolize to FFA which precipitate out
Chalky grey
Following acute pancreatitis or trauma

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12
Q

Fibrinoid necrosis

A

Immune reaction
Antibodies into artery wall and complex with fibrin
Vasculitis (polyarteritis nodosa)

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13
Q

Mechanisms of cell injury

A 
ATP depletion
Mito damage
Ca2+ influx
ROS accumulation
Increased PM perm.
Damaged DNA/misfolded protein accumulation
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14
Q

Apoptosis

A 
Apoptotic bodies (membrane bound)
Pyknotic nucleus
Intrinsic pathway (mito BAX, BAK, caspase 9)
Extrinsic pathway (death receptor, caspase 8)
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15
Q

Autophagy

A

Nutrient stress
Cell eats own contents
Dysregulation indicated in disease

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16
Q

Pathologic Calcifications

A
  1. Dystrophic - dead/dying tissue
    Absence of derangements in Ca metabolism
2. Metastatic - normal tissue
Secondary to derangement in Ca metabolism
Psammoma bodies (indicate turnover)
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17
Q 
Acute Inflammation
(Onset, cell type, tissue injury?, signs?)
A

Fast onset
Neutrophils
Mild tissue injury
Prominent local/systemic signs

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18
Q 
Chronic Inflammation
(Onset, cell type, tissue injury?, signs?)
A

Slow onset
Monocytes/macrophages and lymphocytes
Tissue injury severe
Subtle local/systemic signs

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19
Q

4+1 signs of inflammation

A 
Calor (warmth)
Rubor (erythema)
Tumor (swelling)
Dolor (pain)
Loss of function
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20
Q

5 Agents that cause acute inflammation

A 
Infections
Tissue necrosis
Trauma
Foreign Material
Immune Reactions
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21
Q

Hallmarks of inflammation

A

Vasodilation and vascular permeability

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22
Q

2 receptor families for acute inflammation

A

TLRs (TNF, Type I interferon)

Inflammasome (IL-1)

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23
Q

Exudate

Cause, protein, LDH, cells, specific gravity, glucose

A 
Result of increased vascular permeability
High protein content/ratio
High LDH ratio
High cell content
High specific gravity
Low glucose ratio
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24
Q

Transudate

Cause, protein, LDH, cells, specific gravity, glucose

A 
Result of hydrostatic/osmotic pressure changes
Low protein content/ ratio
Low LDH ratio
Low cell content
Low specific gravity
High glucose ratio
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25
2 vessel changes leading to exudate and mechs
1. Increased blood flow (histamine on smooth muscle) 2. Increased vessel permeability a. Endothelial contraction (hista, bradykinin then IL1/TNF) b. Injury c. Transcytosis (vesicle transport)
26
4 Phases of Leukocyte recruitment
1. Margination/rolling (selectins - hista, IL-1) 2. Adhesion (integrin activation, integrin r exp: IL-1, TNF) 3. Transmigration (diapedesis, BM breakdown) 4. Chemotaxis (IL-8, C5a, LT-B4, bacterial products)
27
4 functions of leukocyte activation
1. Phagocytosis 2. Degradation of engulfed (intra) 3. Secretion of degradation material (extra) 4. Produce inflammatory mediators (TNF, IL-1)
28
Outcomes of inflammation
Resolution (limited tissue destruction) Transition to chronic (not all preceded) Scarring (significant tissue destruction or no regeneration)
29
Main processes of chronic inflammation
``` MNC infiltrate (not neutrophils) Tissue destruction Repair (angiogenesis/fibrosis) ```
30
Characteristic settings for inflammation
Persistent infections Immune-mediated disease Prolonged exposure to toxins
31
4 causes of granulomatous infections
1. Organisms not typically eradicated (TB, fungi) 2. Immune-mediated disease (Crohn's) 3. Foreign material (suture) 4. Sarcoidosis
32
4 roles of macrophages
1. Ingest microbes/debris 2. Initiate tissue repair (often fibrosis) 3. Secrete inflammatory mediators 4. Present antigens
33
Classical macrophage activation (M1) | Activate, produce, function
Activated by: endotoxin, IFN-gamma (T-cells), Foreign mat Produce: ROS, NO, lyso enzyme, pro-inflam cytokines Function: Kill microbes, chronic inflammation
34
Alternative macrophage activation (M2) | Activate, produce, function
Activated by: IL-4, IL-13 (T-cells, eosinophils, mast cells) Produce: GF for angiogenesis and fibroblast activity Function: Tissue repair, fibrosis, wall off
35
Th1 secretions/activation
IFN-gamma | Activates M1
36
Th2 secretions/activation
IL-4 and IL-5 | Activates M2 and eosinophils
37
Eosinophil inflammatory reactions
``` Parasitic infections (toxic to parasites) Allergic reactions (IgE) ```
38
Mast cells
Involved in both chronic and acute inflammation Release histamine and AA Coated/activated by IgE Allergic reactions, quick response to infection
39
Three proteins to measure inflammation
IL-1 IL-6 TNF
40
Cells of chronic inflammation
Macrophages Lymphocytes Eosinophils Mast cells
41
Neutrophilia, Lymphocytosis, Eosinophilia, Leukopenia associated infections
Neutrophilia: bacterial infections Lymphocytosis: viral infections Eosinophilia: asthma, parasitic infections Leukopenia: specific infections (Typhoid)
42
Prostaglandins
Vasodilation Increased vascular permeability Inhibit platelet aggregation
43
TXA2
Vasoconstriction | Promote platelet aggregation
44
Leukotrienes
Bronchospasm | Increased vascular permeability
45
Lipoxins
Inhibit inflammation
46
Chemotaxis factors
Chemokines (IL-8) C5a LTB4 Bacterial products
47
Opsonins
C3b IgG Mannose binding lectin
48
ROS - phagocytosis
superoxide O2-, H202, OH- iNOS: NO
49
Histamine release factors
C3a, C4a, C5a IgE Cytokines: IL-1, IL-8
50
Th17 secretion/activation
IL-17 Attracts macrophages Increased inflammatory response Th1 from hell
51
PAIN
PGs Bradykinin Substance P
52
Anti-inflammatory mediators
Protease inhibitor (alpha-1-antitrypsin) Complement (C1) Leukotrienes (lipoxins) M2 activation
53
4 Components of Repair and the cell responsible
GF secretion - macrophages Neovascularization - endothelial cell Collagen deposition/remodeling - fibroblast Re-epithelizlization/regeneration - epithelial/hepatocytes
54
Granulation tissue
``` Pink tissue made of: fibroblasts new capillaries loose ECM inflammatory cells (macrophages) ```
55
2 Repair Processes
Epthelium - proliferation of residual cells | Organ regeneration - GFs (TNF, IL-6, EGF)
56
Normal scar
Angiogenesis Granulation tissue (type I collagen) Maturation/remodel (type III collagen) Stable fibrous scar
57
Pathologic scar and 2 types
Excessive collagen Hypertrophic scar - regresses Keloid scar - persists
58
Local factors for adverse repair
infection persistence of insult trauma
59
Systemic factors for adverse repair
nutritional (collagen synth): protein/vit C deficiency metabolic: diabetes, GC (inhibit collagen synth) venous drainage impairment (varicose)
60
Disseminated intravascular coagulation features
Simultaneous thrombosis and hemorrhage Widespread clots that consume factors Acute: bleeding Chronic: clotting
61
White (anemic) infarct
``` Arterial blockage Single blood supply No reperfusion Dense tissue Heart, kidney, spleen ```
62
Red (hemorrhagic) infarct
``` Venous blockage Dual blood supply Yes reperfusion Loose tissue Lung, liver, intestine ```
63
Hypovolemic Shock
Low BV, low Q | Coolness/pallor, tachycardia, decreased urine
64
Septic Shock
SIRS, widespread vasodilation Warm/flushed, hypotension/edema, tachycardia, fever Not responsive to IV fluids

D&D (6 decks)

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