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D&D > Exam 2 - Inflammation/Injury > Flashcards

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
Q

2 vessel changes leading to exudate and mechs

A
  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)
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26
Q

4 Phases of Leukocyte recruitment

A
  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
Q

4 functions of leukocyte activation

A
  1. Phagocytosis
  2. Degradation of engulfed (intra)
  3. Secretion of degradation material (extra)
  4. Produce inflammatory mediators (TNF, IL-1)
28
Q

Outcomes of inflammation

A

Resolution (limited tissue destruction)
Transition to chronic (not all preceded)
Scarring (significant tissue destruction or no regeneration)

29
Q

Main processes of chronic inflammation

A 
MNC infiltrate (not neutrophils)
Tissue destruction
Repair (angiogenesis/fibrosis)
30
Q

Characteristic settings for inflammation

A

Persistent infections
Immune-mediated disease
Prolonged exposure to toxins

31
Q

4 causes of granulomatous infections

A
  1. Organisms not typically eradicated (TB, fungi)
  2. Immune-mediated disease (Crohn’s)
  3. Foreign material (suture)
  4. Sarcoidosis
32
Q

4 roles of macrophages

A
  1. Ingest microbes/debris
  2. Initiate tissue repair (often fibrosis)
  3. Secrete inflammatory mediators
  4. Present antigens
33
Q

Classical macrophage activation (M1)

Activate, produce, function

A

Activated by: endotoxin, IFN-gamma (T-cells), Foreign mat
Produce: ROS, NO, lyso enzyme, pro-inflam cytokines
Function: Kill microbes, chronic inflammation

34
Q

Alternative macrophage activation (M2)

Activate, produce, function

A

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
Q

Th1 secretions/activation

A

IFN-gamma

Activates M1

36
Q

Th2 secretions/activation

A

IL-4 and IL-5

Activates M2 and eosinophils

37
Q

Eosinophil inflammatory reactions

A 
Parasitic infections (toxic to parasites)
Allergic reactions (IgE)
38
Q

Mast cells

A

Involved in both chronic and acute inflammation
Release histamine and AA
Coated/activated by IgE
Allergic reactions, quick response to infection

39
Q

Three proteins to measure inflammation

A

IL-1
IL-6
TNF

40
Q

Cells of chronic inflammation

A

Macrophages
Lymphocytes
Eosinophils
Mast cells

41
Q

Neutrophilia, Lymphocytosis, Eosinophilia, Leukopenia associated infections

A

Neutrophilia: bacterial infections
Lymphocytosis: viral infections
Eosinophilia: asthma, parasitic infections
Leukopenia: specific infections (Typhoid)

42
Q

Prostaglandins

A

Vasodilation
Increased vascular permeability
Inhibit platelet aggregation

43
Q

TXA2

A

Vasoconstriction

Promote platelet aggregation

44
Q

Leukotrienes

A

Bronchospasm

Increased vascular permeability

45
Q

Lipoxins

A

Inhibit inflammation

46
Q

Chemotaxis factors

A

Chemokines (IL-8)
C5a
LTB4
Bacterial products

47
Q

Opsonins

A

C3b
IgG
Mannose binding lectin

48
Q

ROS - phagocytosis

A

superoxide
O2-, H202, OH-
iNOS: NO

49
Q

Histamine release factors

A

C3a, C4a, C5a
IgE
Cytokines: IL-1, IL-8

50
Q

Th17 secretion/activation

A

IL-17
Attracts macrophages
Increased inflammatory response
Th1 from hell

51
Q

PAIN

A

PGs
Bradykinin
Substance P

52
Q

Anti-inflammatory mediators

A

Protease inhibitor (alpha-1-antitrypsin)
Complement (C1)
Leukotrienes (lipoxins)
M2 activation

53
Q

4 Components of Repair and the cell responsible

A

GF secretion - macrophages
Neovascularization - endothelial cell
Collagen deposition/remodeling - fibroblast
Re-epithelizlization/regeneration - epithelial/hepatocytes

54
Q

Granulation tissue

A 
Pink tissue made of:
fibroblasts
new capillaries
loose ECM
inflammatory cells (macrophages)
55
Q

2 Repair Processes

A

Epthelium - proliferation of residual cells

Organ regeneration - GFs (TNF, IL-6, EGF)

56
Q

Normal scar

A

Angiogenesis
Granulation tissue (type I collagen)
Maturation/remodel (type III collagen)
Stable fibrous scar

57
Q

Pathologic scar and 2 types

A

Excessive collagen
Hypertrophic scar - regresses
Keloid scar - persists

58
Q

Local factors for adverse repair

A

infection
persistence of insult
trauma

59
Q

Systemic factors for adverse repair

A

nutritional (collagen synth): protein/vit C deficiency
metabolic: diabetes, GC (inhibit collagen synth)
venous drainage impairment (varicose)

60
Q

Disseminated intravascular coagulation features

A

Simultaneous thrombosis and hemorrhage
Widespread clots that consume factors
Acute: bleeding
Chronic: clotting

61
Q

White (anemic) infarct

A 
Arterial blockage
Single blood supply
No reperfusion
Dense tissue
Heart, kidney, spleen
62
Q

Red (hemorrhagic) infarct

A 
Venous blockage
Dual blood supply
Yes reperfusion
Loose tissue
Lung, liver, intestine
63
Q

Hypovolemic Shock

A

Low BV, low Q

Coolness/pallor, tachycardia, decreased urine

64
Q

Septic Shock

A

SIRS, widespread vasodilation
Warm/flushed, hypotension/edema, tachycardia, fever
Not responsive to IV fluids

D&D (6 decks)

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