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General Pathology > Cell Death > Flashcards

Cell Death Flashcards

1
Q

Morphological differentiation in reversibly injured and irreversibly injured cells

A

Reversibly injured:

  • Hydropic degeneration: cisternae of ER swell, Mitochondria swell and round up
  • Ribosomes detach from ER
  • Blebs of plasma membrane

Irreversibly injured:

  • Severe swelling of mitochondria with large densities in mitochondrial matrix
  • Injured lysosomal membranes - enzymes leak out and digest self
  • Injured plasma membrane - proteins leak out
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2
Q

Do irreversibly injured cells have nuclei

A

No

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3
Q

How long after cell injury can light microscopic change be seen

A

Few mins/hours later

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4
Q

How long after cell injury can gross morphological changes be seen

A

Few days later

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5
Q

Appearance of cells dying by necrosis

A

Swelling - cell and internal organelles like mitochondria balloons and ruptures
Inflammation - circulating macrophages and polymorphs converge and phagocytose the necrotic cell
Occurs in large groups
Messy
Disorganised

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6
Q

Morphology of Necrosis

A

Increased eosinophilia - Loss of RNA (more pinkish)
Glassy homogenous cytoplasm - Loss of glycogen
Calcification (dystrophic) - dead cells
Nuclear changes

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7
Q

Describe the different types of Nuclear changes possible

A

Karyolysis: lysing of nucleus due to action of DNAse and RNAse causing fading of basophilia (loss of RNA hence less blue)
Karyorrhexis: fragmentation of nucleus
Pyknosis: condensation of the nucleus and clumping of chromatin (nuclear shrinkage and increased basophilia hence more blue)

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8
Q

Types of Necrosis + examples

A
  1. Coagulative - Myocardial/Renal Infarction
  2. Liquefactive - Stroke/Abscess (brain, renal)
  3. Fat - Pancreatitis/Injury to breast
  4. Caseous - Tuberculosis
  5. Fibrinoid - Hypertension (blood vessels)
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9
Q

What causes Fat Necrosis?

A

Action of digestive enzymes of adipose cells causing the release of fatty acid precipitates

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10
Q

What does Caseous Necrosis look like

A

Gray-white, soft, cheese like

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11
Q

What causes Fibrinoid necrosis?

A

Damage to blood vessels cause increased permeability to proteins, causing plasma proteins to accumulate in the wall making it highly eosinophilic

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12
Q

Which type of necrosis cause highly eosinophilic cells

A

Coagulative Necrosis, Fibrinoid Necrosis

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13
Q

Which type of necrosis causes cell outlines to not be retained/no residual tissue architecture

A

Liquefactive Necrosis, Caseous Necrosis

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14
Q

What are the main differences between Necrosis and Apoptosis

A

Necrosis:

  • Messy and disorganised
  • Inflammation
  • Not cleared
  • Occurs in a large group with neighbouring cells

Apoptosis:

  • Tightly regulated intracellular program, Tidy
  • No/Minimal inflammatory reaction
  • Rapidly cleared
  • Phagocytosed by neighbours
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15
Q

Positive results of apoptosis

A
  1. Destruction of cells during embryogenesis (eg. organogenesis) - prevent malformation
  2. Involution of hormone-dependent tissues (eg. endometrial cell breakdown)
  3. Cell loss in proliferating cell populations (eg. immature lymphocytes that fail to express useful antigens)
  4. Elimination of potentially harmful self-reactive lymphocytes
  5. Death of host cells that have served their useful purpose (eg. neutrophils)
  6. Deletion of activated mature ‘T’ cells at the end of immune response
  7. Killing of virus infected cells/cancer cells (by cytotoxic T cells/ NK cells)
  8. Killing of inflammatory cells (at immunoprivileged sites)
  9. Killing of DNA damaged cells - prevent mutations and cancer
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16
Q

Negative results of apoptosis

A
  1. DNA damage (eg. radiation)
  2. Accumulation of misfolded proteins (eg. degenerative diseases of CNS)
  3. Cell death (eg. viral infections)
  4. Pathologic atrophy in parenchymal organs (eg. duct obstruction in pancreas)
  5. Unscheduled apoptosis of neurons can cause disease (Parkinson’s or Lou Gherig)
17
Q

What cellular observation can be found in apoptotic viral hepatitis cells

A

Councilman bodies

18
Q

What is the sequential ultrastructural changes seen in apoptosis

A
  1. Cell shrinkage
  2. Chromatin condensation
  3. Cytoplasmic blebs and apoptotic bodies (split up)
  4. Phagocytosis of cell bodies by macrophages
19
Q

Mechanism of Apoptosis

A
  1. Initiation Phase (Extrinsic + Intrinsic) - activates caspases
  2. Execution phase - proteolytic cascade
20
Q

Explain the Extrinsic Initiation pathway of Apoptosis

A
  1. Ligand binding to death receptor on cell surface (TNF-a binding to the TNF-a receptor; Fas binding to CD95)
  2. Receptors cluster acitvating caspase 8
  3. Caspase 8 activates Caspase 3
  4. Caspase 8 and 3 cleave apoptotic substrates
21
Q

Explain the Intrinsic Initiation pathway of Apoptosis

A
  1. DNA damage induces p53
  2. p53 induces Bax protein synthesis
  3. Bax promotes release of cytochrome C from the mitochondria
  4. Cytochrom C in the cytosol activates Caspase 9
  5. Caspase 9 activates Caspase 3
22
Q

Explain the Execution pathway of Apoptosis

A

Caspases are cysteine proteases which selectively cleave target proteins (eg. Caspase-activated DNase (CAD) - cuts DNA between nucleosomes)

23
Q

What is the difference in diffusion analysis of Apoptotic cells vs Necrotic cells

A

Apoptosis: Ladder pattern
Necrotic: Diffuse Smearing

24
Q

How do apoptotic cells target themselves?

A

Phosphatidyl Serine moves from the inside to the outside leaflet of plasma membrane of apoptotic cells
Annexin I protein is released by the cell as a result of caspase activation to bind to PS on the cell surface as an “eat me” signal

25
Q

What drug promotes apoptosis?

A

Bcl-2 antisense (G3139) blocks Bcl-2 production which encourages apoptosis and shows anti-tumour effect for malignant melanoma patients

26
Q

What drug inhibits apoptosis

A

Caspase inhibitors which is effective for ischaemia-reperfusion injury, traumatic brain injury, Parkinson’s disease, Bacterial meningitis, Huntington’s Alzheimer’s disease

27
Q

What are the types of Intracellular accumulations

A
  1. Lipids
  2. Protein
  3. Glycogen
  4. Pigment
28
Q

Types of Lipid Storage disorders

A
  1. Steatosis or Fatty change (accumulation of triglycerides in liver/heart/muscle/kidney)
  2. Inherited lysosomal storage disorders - Cerebrosides in Gaucher’s disease, Gangliosides in Tay-Sach’s disease, Mucopolysaccharides in Hunter and Hurler syndromes
  3. Accumulation of cholesterol-laden macrophages - Atherosclerosis (arteries), Xanthomas (skin), Cholesterolosis (Gall bladder)
29
Q

Types of Protein Storage disorders

A
  1. Mallory’s hyaline (pink stained inclusion bodies containing cytokeratin and ubiquitin in liver cells)
  2. Amyloidosis (congo-red stain both intra and extra cellular accumulation of protein)
  3. Alpha-1-antitrypsin deficiency (slowed folding and accumulation of enzyme in liver cell ER, failing to be secreted to protect the lungs from Neutrophil Elastase)
30
Q

Types of Glycogen Storage disorders

A
  1. Uncontrolled diabetes (enlarged hepatocytes)

2. Inherited defects of glycogen metabolism (glycogen storage disease)

31
Q

Types of Pigment Storage Disorders

A

A. Endogenous

  1. Haemosiderin Accumulation (granular yellow-brown pigment in liver, pancreas and heart)
  2. Lipofuschin Accumulation (Fine, granular, yellow-brown pigment of lipid complexed to protein)

B. Exogenous

  1. Coal dust - causes Anthracosis (blackening of lungs)
  2. Tattooing (inoculated pigments are phagocytosed by dermal macrophages)
32
Q

Types of pathologic Calcification

A
  1. Dystrophic Calcification (abnormal deposition of calcium phosphate in dead or dying tissue) - atherosclerotic disease, valvular heart disease)
  2. Metastatic Calcification ( calcium deposition in normal tissues due to hypercalcemia: increased PTH with subsequent bone resorption, bone destruction, Vit D disorders, Renal failure with secondary increase in PTH)
33
Q

What do microcalcifications in the breast signify

A

Cancer. Necrosis of tumour cells attract calcium.

General Pathology (10 decks)

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