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Pathology F2014 > Cell injury > Flashcards

Cell injury Flashcards

1
Q
A

Histopathologic features of reversible cell injury

  • Cell swelling
  • Blebs on cell surface and microvilli
  • Myelin figures
  • Swollen mitochondria
  • Darker staining
  • cells switch from aerobic respiration to anaerobic glycolysis
  • depletion of ATP
  • glycogen depletion
  • lactic acid accumulation
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2
Q
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​Histopathologic features of irreversible cell injury

  • loss of nuclei
  • severe vacuolization of mitochdondria
  • swollen lysosomes
  • Massive Ca2+ influx causing protein denaturation and coagulative necrosis via phospholipases, proteases, and endonucleases
  • loss of phospholipids
  • lipid breakdown products
  • cytoskeletal alterations
  • Saponification due to accumulation of Ca2+
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3
Q

Types of necrosis

A
  1. Coagulative necrosis: necrosis of solid tissue (heart, spleen, kidney), coagulated cells, proteins of cells are denatured however cell shape and size preserved
    - cause: ischemia
  2. Fat necrosis: chalky-cheese appearance; divided into non-traumatic and traumatic, Ex. pancreas (from lab)
  3. Liquefactive necrosis: occurs in brain (only type) and lungs
    - cause: hydrolytic enzymes & bacteria
  4. Caseous necrosis: cheesy-milk, eosinophilia, granulomas (dead macrophage), Ex lung (from lab)
    - cause: only TB
  5. Gangrenous necrosis: combination of ischemic coagulative necrosis & wet gangrene, clot in arteries causing hypoxia in limbs and heart
    - cause: ischemia
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4
Q

Intracell accumulation of lipids

A
  • liver & heart are best examples, but any tissue can be affected
  • fatty change often has little or mild functional effects; Exception is CCl4 change in lipid accumulation
  • Fatty change in heart usually secondary to prolonged hypoxia or diptheric myocarditis
  • Xanthoma: cholesterol-filled macrophages
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5
Q

Hypertrophy

A
  • increase in size of cell accompanied by augmented functional capacity
  • causes: increased functional demand
  • Ex. LVH in hypertension
  • Ex2. muscle hypertrophy in athletes
  • Ex3. sex organs at puberty
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6
Q

Hyperplasia

A
  • increase in number of cells
  • Causes: increased functional demand
  • Ex. polycythemia vera in high altitudes
  • Ex2. endometrium in early phase of menstrual cycle
  • Ex3. skin in calluses
  • Ex4. Benign Prostatic Hyperplasia/Hypertrophy (BPH:) urethral compressed by many nodules
    Ex5. Physiologically, hyperplasia in breasts during pregnancy and lactation
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7
Q

Metaplasia

A
  • conversion of one cell type to another
  • Ex1. bronchial ciliated columnar to squamous metaplasia in smokers
  • Ex2. vagina/cervix (Cuboid to S; squamous metaplasia),
  • Ex3. gall bladder (transitional to squamous metaplasia)
  • Ex4. urinary bladder (transitional to squamous metaplasia)
  • Ex5. GERD (squamous to columnar cell metaplasia)
  • Ex6. Keratomalacia
  • Ex7. Myositis ossificans
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8
Q

Dysplasia

A
  • alteration in size, shape, and organisation of cell components including nuclei
  • pre-neoplastic lesion
  • Cause: persistent injury
  • Ex. dysplasias in bronchial epithelium, cervical epithelium (CID), uterine epithelium
  • dyplasias are graded
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9
Q

Exudate

A
  • rich in proteins and cells
  • specific gravity > 1.02
  • classify inflammation based on contents of exudate ex. bacteria
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10
Q

Pus

A
  • exudate of PMN, cell debris, and lysosomal enzymes
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11
Q

Transudate

A
  • outpouring of fluid w/ low protein
  • specific gravity <1.012
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12
Q

Changes in vascular flow & calibre: Triple response of Lewis

A
  1. pale line along area of stroke
  2. Flare
  3. Swelling w/ blanching

w/ time-lapse

  1. Transient vasoconstriction of arterioles
  2. vasodilatation
  3. permeability changes w/ exudation:
  4. As blood flows more slowly and becomes more viscous, cell events begin to take place
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13
Q

Endothelial cells capable of secreting:

A
  • prostaglandins
  • coagulant factor VIII
  • collagens
  • anticoagulants (plasminogen activator)
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14
Q

5 mechanisms by which the endothelium becomes leaky during inflammation

A
  1. Immediate transient response: Leaky endothelium due to histamine inducing endothelial muscle contraction -> vasodilation -> and widening the space b/w endothelial cells.
  2. Junctional retraction: cytokine mediated, reorganization of cytoskeleton, disruption of endothelial cells, occurs 4-6 h post-injury, lasts > 24 h, demonstrated w/ TNF and IL-1 experimentally
  3. Direct endothelial injury w/ endothelial cell necrosis and detachment: endothelial detachment secondary to platelet adhesion and thrombosis, can either be immediate sustained or delayed prolonged leakage
  4. Leukocyte dependent endothelial injury: involves toxic O2 species and endothelial cell detachment occuring mostly in venules and pulm. capillaries
  5. Increased transcytosis: occurs in presence of VEGF, increase venular permeability
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15
Q

Migration of Leukocytes (Exudation) sequence of events

A
  1. margination: WBC (smaller) pushed to periphery
  2. pavement & rolling: interaction of CAM on leukocyte (L-selectin) and endothelial cell surfaces (P-selectin & E-selectin)
  3. adhesion & emigration: mediated by endothelial adhesion molecules binding to integrins, ICAM-1 & VCAM (both upregulated) w/ LFA-1 (CD11a/18) & Mac1 (CD11b/18) and VLA-4, respectively
  4. chemotaxis & activation: bacterial products, C5a, LTB4, chemokines
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16
Q

Phagocytosis involves 3 steps

A
  1. Recognition & attachment: involves opsonisation and attachment to 2 receptors on PMN or macrophages. Properties of macrophages:
    - highly motile
    - receptor for IgG and C3b
    - activation by external stimuli
  2. Engulfment: process involving pseudopods, phagolysosome, Ca2+, Mg2+
  3. Killing and/or degradation: 2 types of bactericidal mechanisms
    a. O2-dependent mechanisms:
    - H202-myeloperoxidase-haide system; mechanism deficient in Pt w/ chronic granulomatous disease; final reactive radical is HOCl
    - MPO-independent killing; OH free radical
    b. O2-independent bactericidal mechanisms
    - decreased pH from lactate, carbonic anhydase actiivty, acid hydrolases w/in phagolysosome
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17
Q

During phagocytosis, leukocytes release products extracell. in 3 ways

A
  1. Regurgitation during feeding
  2. Reverse endocytosis (frustrated phagocytosis)
  3. Cytotoxic release (following cell death)
18
Q

Neurogenic mechanisms

A
  • brief vasoconstriction in very early phaes of inflammtory rxn
  • blocked by anesthesia
  • followed by antidromic reflex w/ inhibition of vasoconstriction leading to vasodilation
  • absence of innervation does not prevent inflammation
19
Q

Chemical mediators of inflammation: cell-derived

A

a. arachidonic acid metabolites: Prostaglandins & Leukotrienes
b. PAF: vasodilator, increases permeability, platelet aggregation; generated by all inflammatory cells, endothelial cells, and damaged cells.
c. vasoactive amines: 5HT (present on platelets only) & histamine -> vasodilates, increases venule permeability

20
Q

Agents responsible for release of histamine

A
  1. physical: trauma, cold
  2. immunologic (via IgE receptors)
  3. C3a and C5a (anaphylatoxins)
  4. histamine releasing factors from PMN, monocytes, and platelets
  5. IL-1

Note: degranulation mediated by cAMP and stimulated by platelet contact w/ collagen, thrombin, AFP, and Ag-Ab

21
Q

Chemical mediators of inflammation: plasma derived vasoactive mediators

A

3 different but interrelated systems:

  1. complement system
  2. clotting system
  3. kinin system: Bradykinin increases vascular permeability, produces smooth muscle contraction, vasodilation, and pain.
22
Q

Acute & chronic inflammation

A
  • no sharp line
  • Acute: 5 cardinal signs, vascular and exudative, characterized by presence of PMN
  • Chronic: great amount of cell proliferation and CT, while less exudation; arbitrarily set at 2- 4 wks clinically
  • Histopath of chronic inflammation: Ex. chronic inflammation of kidney; tubules far apart
  • Chronic inflammation can occur from:
    • persistent acute inflammation that is not resolved: Ex. PUD
    • de novo inflammation: Ex. TB
  • Chronic subdivided into 2 forms:
  • Non-specific chronic inflammation: characterized by mononuclear cells & CT cells (fibroblasts)
  • Granulomotous inflammation: characteristic tissue reactions in some infections (TB, syphillis, cat-scratch disease, fungal; protozoan), persistent forgein body inflammations, rheumatic fever (Aschoff body); rheumatoid arthritis, sarcoidosis, granuloma annular of skin
    • Hallmark: epithelioid histiocyte surrounded by Giant cells
23
Q

Serous inflammation

A
  • albumin-containing exudate
  • serosal mesothelial cells (peritoneal, pleural, pericardial, synovial)
  • causes pitting edema
  • Ex. blister from burns of skin; pulmonary TB
24
Q

Fibrinous inflammation

A
  • severe inflammations -> vessels permitting passage of large size molecule: fibrinogen)
  • Ex. rheumatic fever (bread & butter pericarditis) and in pneumococcal pneumonias
  • In tissues: easily identifiable b/c the ppt fibrin is deeply acidophilic
25
Q

Suppurative or purulent inflammation

A
  • a type of liquefactive necrosis
  • characteristically seen in pyogenic infections by: staphylococcus, pneumococcus, miningococcus, gonococcus, E. coli, some non-haemolytic strep
  • Ex. acute appendicitis
  • In tissue: recognized by pools of numerous polyps (viable and dead)
26
Q

Sanguinous inflammation

A
  • exudate containing a large number of RBCs
  • Ex. often seen in TB (sanguinous pleuritis)
  • Ex2. inflammations as reactions to tumor invasion (sanguinous pericarditis)
  • Ex3. Can also result from frost bites
27
Q

Abscess

A
  • caused by great intensity irritant (staph, turpentine)
  • localised collection of pus caused by suppuration
  • hole in tissue due to trypsin digestion, many PMN
28
Q

Erysipelas

A
  • facial rash
29
Q

Paronychia

A
  • infections of fingernail
30
Q

Felon

A
  • infection of distal phalanx
31
Q

Empyema

A
  • collection of pus in pleural cavity
32
Q

Ulcer

A
  • epithelium defect or excavation
  • produced by sloughing of inflammatory necrotic tissue on surface
33
Q

Pseudomembranous inflammation

A
  • inflammation produced by powerful necrotizing toxin such as diphtheria
  • false membrane consists of ppt fibrin, necrotic epithelium, and WBC
  • pharynx, larynx, GI tract
34
Q

Defects in leukocyte migration and chemotaxis

A

a. intrinsic corpuscular abnormality: Chediak-Higashi syndrome, diabetes
b. extrinsic

  • defect in production of chemotactic factors (C5 deficiency)
  • serum chemotactic inhibitors (C5 inactivators, especially in cirrhosis, sarcoidosis)
  • inhibitors of leukocyte locomotion
  • drugs
  • factors in malignancy
  • rheumatoid arthritis
35
Q

Defects in microbicidal activity

A
  • impaired H2O2 production: CGD
  • MPO deficiency
  • severe G6PD deficiency
36
Q

Mechanisms involved in regen & repair: control of cell proliferation

A
  1. stimulatory hormones & growth factors
  2. inhibitory factors (chalones): lost of epidermal, granulocyte, lymphocyte chalones during injury
  3. cell-cell interactions
  4. cell-matrix interactions: integrin family (fibronectin-R, platelet surface-R, CAM)
37
Q

Mechanisms involved in would healing: Fibronectins

A
  • most important in wound healing; binds to both ECM components and cell surfaces -> crazy glue or bridge
  • seen in cell surfaces, BM, pericell matrices
  • facilitate migraiton of new epithelium, chemotactic for monocytes and fibroblasts
  • glycoprotein
  • produced by fibroblasts, monocytes, endothelial cells
38
Q

Collagenization & wound strength

A
  1. angiogenesis: VEGF & b-FGF
  2. Fibrosis: proliferation of site fibroblasts and deposition of ECM
  3. Maturation and organisation of scar: collagen and other ECM degraded by metalloproteinases (zinc dependent)
39
Q

Skin wound healing

A
  1. Crust formation: provisional closure
  2. Removal of dead tissue: w/ line of zone of demarcation
  3. Replacement of lost cell and tissues: new tissue containing proliferating cellular and ECM termed Granulation tissue (tiny pink granules)
40
Q

Stages of wound closure

A
  • latent period: size of wound does not change
  • period of contraction: shrinkage of granulation tissue -> edges are pulled together
  • epidermization
41
Q
A
  • granulomatous inflammation
42
Q

Types of collagen

A
  • adult skin: Collagen type I
  • Granulation tissue: type III
  • Cicatrisation: type III to I leading to wound retraction
  • 5 major types of collagen:
    • Types I, II, & III: fibrillary
    • Types IV & V: amorphous and are found in basement membrane
    • Keloid is type III collagen
    • T1: bONE
    • T2: cart2lage
    • T3: pliability (embryonic tissue)

Pathology F2014 (17 decks)

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