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Pathology MBBS > Cell injury,death,adaptations & acute inflammation > Flashcards

Cell injury,death,adaptations & acute inflammation Flashcards

1
Q

Most common cell injury
Most common cause of hypoxia
Cells most sensitive to hypoxia
Cells least sensitive to hypoxia

A

Hypoxia

Ischemia

Neuron

Fibroblasts, then skeletal muscles

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2
Q

Major organelles affected by cell injury

A
  1. Nucleus
  2. Mitochondria (most commonly affected by reversible cell injury)
  3. Plasma membrane
  4. RER
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3
Q

Etiology

A

Initiating cause of the disease

Genetic ,environmental or both

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4
Q

Anorexia nervosa

A

Extreme self imposed food restriction

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5
Q

Hydropic change or vacuolar degeneration

A

Cellular swelling which is the earliest manifestation of almost all forms of injury to the cell

Small clear vacuoles which represent distended and pinched off segments of ER are present

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6
Q

Changes in the staining of cells progressing towards necrosis

A

The cytoplasm becomes more eosinophilic due to:

  1. loss of RNA
  2. Accumulation of denatured proteins
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7
Q

What are DAMPs

A

Damage associated molecular patterns

Include ATP (from mitochondria), uric acid (breakdown product of nucleus) and other molecules which are usually present within the cell and whose release is an indicator of severe cell injury.
They trigger phagocytosis and cytokine release
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8
Q

Hypertrophy

A

Increase in cell size due to increased production of cellular proteins
Usually in permanent cells

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9
Q

Examples of hypertrophy

A 
1. Pathologic hypertrophy (via 
Enlargement of heart
2. Physiologic hypertrophy
Growth of uterus
Body builders

Due to increased cellular protein production

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10
Q

Mechanisms of hyperplasia

A
  1. Growth factor driven proliferation

2. Stem cell derived (eg., liver cell regeneration)

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11
Q

Examples of physiological and compensatory hyperplasia

A

Physiological:
puberty, pregnancy, lactation
Compensatory:
partial hepatectomy, nephrectomy

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12
Q

Examples of pathological hyperplasia

A
  1. Hormonal (eg.,endometrial, prostatic)
  2. Viral warts
  3. Wound healing
  4. Bone marrow
  5. Lymphoid tissue
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13
Q

Examples of both hyperplasia and hypertrophy

A

Breast during puberty

And uterus during pregnancy

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14
Q

Atrophy

Mechanism

A

Loss of cell number and size
Mechanism:
1. Decreased protein synthesis
2. Increased protein degradation

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15
Q

Examples of physiological atrophy

A
  1. Thyroglossal duct and notochord

2. Uterine involution

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16
Q

Examples of pathological atrophy

A
  1. Arterial occlusion
  2. Inadequate nutrition
  3. Disuse
  4. Loss of innervation
  5. Pressure atrophy (eg., neoplasms causing compression)
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17
Q

Examples of epithelial metaplasia

A 
1. In airways by cigarette smoke
Pseudostratified to squamous 
2. Urinary bladder by bladder stone
Transitional to squamous
3. Barrett’s oesophagus by gastroesophagial reflux
Squamous to columnar
4. Cervix due to acidity
Glandular to squamous
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18
Q

Vitamin deficiency leading to squamous metaplasia

A

Vitamin A deficiency

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19
Q

Messenchymal metaplasia examples

A 
Osseus metaplasia (eg.,testis)
Eg., myositis ossificans (occurs in athletes as they are more prone to injury)
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20
Q

Necrotic cells have a glassy homogenous appearance relative to normal cells due to

A

Loss of glycogen particles

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21
Q

Ultrastructural changes of reversible cell injury include

A
  1. Cell membrane: Blebbing, blunting and loss of microvilli
  2. Mitochondria: swelling and small amorphous densities
  3. Cytoplasm: myelin figures (phospholipids from damaged cell organelles)
  4. ER: dilation, detachment of polysomes from it
  5. Nucleus: alterations with disaggregations of granular and fibrillar material
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22
Q

Fate of myelin figures

A
  1. Phagocytosed by other cells

2. Further degraded to FA. Calcification of such FA results in deposition of calcium rich precipitates

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23
Q

Types of necrosis

A
  1. Coagulative
  2. Liquefactive
  3. Fat: enzymatic and traumatic
  4. Caseous
  5. Fibrinoid
  6. Gangrene
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24
Q

Necrosis is because of two processes

A
  1. Denaturation of proteins

2. Enzymatic digestion of cells

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25
Q

Necrosis is characterised by electron microscope by

A
  1. Discontinuities in the plasma and organelles membranes
  2. Marked dilation of mitochondria with the appearance of large amorphous densities
  3. Intracytoplasmic myelin figures
  4. Amorphous debris
  5. Denatured proteins as aggregates of fluffy proteins
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26
Q

Coagulative necrosis which causes infarcts

A

The enzymes are also denatures with the structural proteins, hence blocking the proteolysis of dead cells.
Infiltrating leukocytes release lysosomal enzymes
Intensely eosinophillic cells with indistinct reddish nucleus are seen
Eg., Vessel obstruction ischemia except brain

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27
Q

Colliquative/ Liquefactive necrosis

A

Digestion of dead cells occurs, resulting in the transformation to a viscous fluid.
The necrotic material usually forms a creamy yellow pus

Eg.,
bacterial and fungal infections (enzyme release and leukocyte stimulation)
Hypoxic death of cells in CNS
Abscesses

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28
Q

The term cellular pathology was coined by

A

Rudolf Virchow

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29
Q

Gangrene

A

It is a pattern of cell death, applied to a limb (lower leg) that has lost its blood supply and has undergone necrosis (coagulative) involving multiple tissue planes

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30
Q

Wet gangrene

A

When a bacterial infection occurs with gangrene, there is more liquefactive necrosis
So liquifactive necrosis is considered as an example of wet gangrene while coagulative necrosis is considered as an example of dry gangrene

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31
Q

Casseous necrosis

Granuloma

A

The term caseous is derived from the friable white appearance of the area of necrosis
On microscopy, pink granular appearance
(Can be considered as a type of coagulative or combination of coagulative and liquifactive necrosis)
Focus of this necrosis is called granuloma

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32
Q

Fat necrosis - enzymatic

A

In acute pancreatitis, pancreatic lipase leak out of the damaged acinar cells and liquefy the membranes of fat cells in the peritoneum,
releasing TAG esters that are split.
That’s fatty acids combined with Ca to produce grossly visible chalky white areas (fat saponification)
Other examples are mesentery, omentum,…
Example of traumatic fat necrosis is breast

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33
Q

Fibrinoid necrosis

A

When complexes of antigens and antibodies are deposited in the walls of arteries
Type 3 or type 4 hypersensitivity.
This, together with the leaked plasma proteins , results in a bright pink and amorphous appearance in H and E strain called fibrinoid

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34
Q

Physiological examples of apoptosis

A
  1. Removal of excess cells during development
  2. Involution of hormone dependent tissues
  3. Cell turn over in proliferating cell populations
  4. Elimination of potentially harmful self reactive proteins
  5. Death of cells that have served is
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35
Q

Pathological apoptosis

A
  1. DNA damage
  2. Accumulation of misfolded proteins
  3. Infections (viral)
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36
Q

Morphological features of apoptosis

A
  1. Cell shrinkage: eosinophilic (normal-looking organelles which are tightly packed)
  2. Chromatin condenses peripherally into dense masses of various shapes (nucleus may split)
  3. Cytoplasmic blebs and apoptotic bodies
  4. Phagocytosis
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37
Q

Mitochondrial/ Intrinsic pathway of apoptosis upto initiator caspases

A

Cell injury (growth factor withdrawal/ DNA damage/ ER stress) ➡️
BCL2 family sensors ➡️
BCL2 family effectors (BAX,BAK)- Pro-apoptotic➡️
Mitochondrial membrane permeability decreases ➡️
Leakage of cytochrome c and other pro-apoptotic proteins ➡️
Initiator caspases (9)

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38
Q

Death receptor/ Extrinsic pathway of apoptosis

A

Receptor ligand interactions (Fas receptor / TNF receptor)➡️
Adaptor proteins called FADD (FAS Assoc. Death Receptor) ➡️
Initiator caspase activation (8 and 10)

39
Q

Common steps of apoptosis mechanisms

A 
Initiator caspases ➡️
Executioner caspases 3 and 6 (7 also)
➡️ :
1. Endonuclease activation ➡️ nuclear fragmentation 
2. Breakdown of cytoplasm
➡️ 
Cytoplasmic bleb➡️
Apoptotic body ➡️
Phagocytosis
40
Q

Anti apoptotic proteins (having 4 BH domains)

A

BCL2, BCL-XL and MCL1
Located in the outer mitochondrial membrane, cytosol and ER membranes
Prevents leakage of cytochrome c and other death inducing proteins

41
Q

Pro apoptotic proteins (having first 3 BH domains)

A

BAX and BAK (p53 also)
On activation they oligomerise within the outer mitochondrial membrane, increasing its permeability
Thus leakage occurs

42
Q

Regulated apoptosis initiators (have the 3rd BH domain) or arbiters of apoptosis

A

BAD, BIM , BID, Puma and Noxa
Their activity is regulated by sensors of cellular stress and damage
When activation causes apoptosis

43
Q

The critical initiator caspase of intrinsic mechanism which is activated by the apoptosome (cytochrome c ➕ APAF-1)

A

Caspase-9

44
Q

The process of apoptotic cell phagocytosis is called

A

Efferocytosis

45
Q

Necroptosis or programmed necrosis

Mechanism

A

Starts similar to apoptosis (extrinsic) but the caspases are inactive, ending like necrosis
Appears like necrosis
Involves receptor interacting protein kinase 1 and 3 (RIPK -1 and RIPK-3)

46
Q

Examples of necroptosis

A
  1. Formation of mammalian bone growth plate
  2. Cell death in steatohepatits, acute pancreatitis.
  3. Cell death in ischaemia-repurfusion injury
  4. Neurodegenerative diseases like Parkinson’s disease
  5. Backup mechanism of defence against viruses that encode caspase inhibitors (cytomegalovirus)
47
Q

Important cells involved inflammation

A

In acute inflammation it is neutrophil

In chronic inflammation it is monocyte or macrophage

48
Q

Exudate

A

Inflammatory edema
Specific gravity of exudate is more than 1.020
Rich in cells and proteins
LDH is high in exudate

49
Q

Transudate

A

Non inflammatory
Specific gravity less than 1.012
Poor in cells and proteins
Low LDH

50
Q

4 cardinal signs of inflammation

A 
Rubor 
Dolor - pain
Calor
Tumour- swelling
This was given by Celsus

The fifth sign given by Virchow was Functio laesa - loss of function

51
Q

Vascular events of acute inflammation

A
  1. Earliest transient vasoconstriction
  2. Vasodilation and increased vascular permeability
  3. Stasis (of blood flow)
  4. Margination/ pavementing
52
Q

Most critical event or hall mark of acute inflammation

A

The second step

Vasodilation and increased vascular permeability

53
Q

Cellular events of acute inflammation which follows the vascular events

A
  1. Adhesion and transmigration
  2. Chemotaxis
  3. Phagocytosis
54
Q

Mechanisms of increased vascular permeability

A
  1. Endothelial retraction in post capillary venules
  2. Endothelial cell contraction
  3. Direct endothelial injury
  4. Increased transcytosis
55
Q

Endothelial cell retraction

A

Occurs in post capillary venules
Immediate transient response
Mediators: histamine, leukotrienes

56
Q

Endothelial cell contraction

A

Occurs in venules and capillaries
Mediator: IL-1, TNF-alpha
Causes delayed sustained response

57
Q

Direct endothelial injury

A

Mechanism acts on capillaries, venules and arterioles

Two types: severe and mild

58
Q

Severe direct endothelial injury mechanism

A

By severe sunburn, chemicals
Endothelial cells will undergo necrosis and detachment
Leakage of fluid starts immediately
Continue till the new cells regenerate
Responsible for delayed sustained response

59
Q

Mild direct endothelial injury mechanism

A

Endothelial cells undergo apoptosis
Leakage starts after some time
Responsible for delayed sustained response

60
Q

Transcytosis

A

Passage of fluid through the channels which are formed in endothelial cell cytoplasm
Mediator: VEGF Vascular endothelial growth factor

61
Q

Selectins (CD 62)

A

Three types: E (endothelium) ,P (platelet) and L selectin (leukocyte)
Their function is rolling

62
Q

Complementary receptors of various selectins

A
  1. For E and P selectins it is Sialyl Lewis X modified glycoproteins located on the leukocyte
  2. For L selectins it is GLYCAM 1 - CD34
    Involved in rolling
63
Q

Immunoglobulins involved in cellular phase of acute inflammation

A
  1. ICAM-1 interacts with beta 2 integrin
  2. VCAM-1 interacts with beta 1 integrin
    Both present on the endothelium
    Involved in adhesion
64
Q

Integrins involved in cellular phase of acute inflammation

A
  1. Beta 2 integrin (CD 2 / CD-18) (LFA 1 / MAC 1)
  2. Beta 1 integrin (VLA-4)

Present in the leukocyte
Involved in adhesion

65
Q

CD 31

A

Also called PECAM 1
It brings out transmigration of the cellular phase of acute inflammation
Movement of leukocyte out of the endothelium

66
Q

Mechanism of appearance of adhesion molecules

A
  1. Redistribution: for P selectin
  2. Induction:
    ICAM-1, VCAM-1, E selectin
    Fresh synthesis mediated by IL-1 and TNF-alpha
  3. Increased avidity of binding:
    Integrins
    Increased number and strength of binding
67
Q

Mechanism of appearance of p selectin

A

Redistribution
P selectin is present in the Weibel palade bodies of endothelium
During inflammation mediators like histamine, thrombin, PAF lead to the release of P-selectin to the surface of endothelium

68
Q

Examples of exogenous chemotactic factors

A

Bacterial cell wall proteins like N Formyl Methionine

69
Q

Examples of endogenous chemotactic factors

A
  1. C5a (a complement factor)
  2. LTB4 (a leukotriene)
  3. IL-8 (a interleukin)
70
Q

Mechanism of chemotaxis

A

7 transmembrane G protein coupled receptors ➡️ increased cytosolic Ca ➡️ polymerisation of actin
➡️ chemotaxis

71
Q

The receptors for recognition and attachment for phagocytosis

A
  1. Mannose receptors
  2. MAC 1 receptor
  3. Scavenger receptors
72
Q

Which substances can act as opsonins

A
  1. Fc fragment of IgG
  2. C3b complementary protein
  3. Serum proteins like fibrinogen, CRP,…
73
Q

Pyroptosis

A

Form of apoptosis accompanied by fever inducing cytokine IL-1 involving inflammosome and caspase 1
Thought to be the mechanism of microbial infection

74
Q

Mechanism of pyroptosis

A

Microbial products that enter infected cells are recognised by cytoplasmic innate immune receptors
➡️ multiprotein complex called inflammasome is activated
➡️ activation of caspase-1 (also caspases 4 and 5)
➡️ activation of IL-1
➡️ inflammation (leukocyte recruitment and fever)

75
Q

Ferroptosis

A

Caused when excessive intercellular iron or ROS overwhelm glutathione-dependent antioxidant defences
Lipid peroxidation ➡️ loss of membrane permeability
Cell death similar to necrosis, but regulated by specific signals and can be prevented by reducing iron levels

76
Q

Ultrastructural features and examples of ferroptosis

A

Loss of mitochondrial cristae
Ruptured outer mitochondrial membrane

Variety of human pathologies like cancer, neurodegenerative diseases, stroke

77
Q

Oxygen dependent killing

A

Most important
Also called oxidative burst
1. O2➡️ superoxide ion by NADPH oxidase
2. Hydrogen peroxide is formed which combines with chloride to form hypochlorite
Most effective bacterial killing system is the hydrogen peroxide halide system

78
Q

Oxygen independent killing

A

Mediated by lysosomal enzymes like lysozyme, lactoferrin, BP1 (bacterial permeability increasing proteins)

79
Q

LAD 1 or leukocyte adhesion

A 
Autosomal recessive
Defect in beta 2 integrin
1. Recurrent infections
2. Delayed separation of umbilical cord
3. Delayed wound healing
80
Q

LAD 2

A

Mutation in sialyl Lewis X modified glycoprotein
Delayed rolling and adhesion
Recent infections

81
Q

Chronic granulomatous disease CGD

A

X linked recessive (75%) or autosomal recessive (25%)
Deficiency of NADPH oxidase
Recurrent infection with catalase positive organisms
Test: Nitro Blue Tetrazolium test (NBT)

82
Q

Chediak Higashi syndrome

A

Autosomal recessive

Mutation of LYST protein required for phagolysosome fusion

83
Q

Emperipolesis

A 
Intact viable cell within a cell
The cell can exit without any structural or morphological change
Seen in:
1. Rosai Dorfman syndrome
2. Hematolyphoid disorders like CLL
3. NHL
84
Q

Chediak Higashi syndrome characteristics

A
  1. Fever
  2. Recurrent infections
  3. Albinism
  4. Deafness
  5. Thrombocytopenia
  6. Giant granules in neutrophils
85
Q

Neutrophil extracellular traps NETs

A

Extracellular fibrillar mesh work produced by neutrophils at the site of infection
Provide a high concentration of antimicrobial substances at the infected site
Arginine is involved

86
Q

Myelin figures are seen in

A

Both reversible and irreversible cell injury, though more in irreversible cell injury

87
Q

Characteristics of irreversible cell injury

A
  1. Profound disturbances in cell membrane:
    Becomes completely permeable, so cytosolic Ca increases➡️ activation of phospholipase, proteases,…
  2. Severe mitochondrial damage
  3. 3 nuclear changes
  4. Release of lysosomal enzymes
88
Q

Most common morphological features of irreversible cell injury

A

Flocculent amorphous densities in mitochondria (on electron microscopy)
In light microscopy it is the nuclear changes

89
Q

Special features of coagulative necrosis

A

Most common type of necrosis

Most common organ affected by coagulative necrosis is heart

90
Q

Examples of coagulative necrosis

A

Hypoxia
Severe burns
Zenker’s degeneration (patients with severe toxaemia like typhoid, affecting muscles like rectus abdominis and diagram)

91
Q

Microscopy of coagulative necrosis

A
  1. Cell architecture/ outline is preserved
  2. Cells become eosinophilic
  3. Cells have glossy appearance due to loss of glycogen
  4. Cells have moth eaten appearance due to loss of organelles.
92
Q

Examples of caseous necrosis

A
  1. TB (mycolic acid has high fat content)

2. Final infections like histoplasmosis, coccidiomycosis

93
Q

Examples of fibrinoid necrosis

A
  1. Ascoff nodules
  2. Poly arteritis nodusa/ vasculitis
  3. Malignant hypertension

Pathology MBBS (17 decks)

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