Cell Injury Flashcards

1
Q

What is reversible cell injury?

A

Cells adapt to changes in environment - return to normal upon removal of stimuli

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2
Q

What is Irreversible cell injury?

A

Permanent - cell death

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3
Q

What are the causes of cell injury (=aetiology)?

A

Hypoxia
Ischaemia
Physical agents
Chemicals/drugs
Infections
Immunological reactions
Nutritional imbalance
Genetic defects

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4
Q

What is Hypoxia?

A

O2 deficiency
Disrupting oxidative respiratory processes
Anaerobic mechanism engage

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5
Q

What is Ischaemia?

A

Reduced blood supply
Caused by atherosclerosis
Hypoxia + Nutrient deficiency
More severe

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6
Q

How physical agents may cause cell injury?

A

Mechanical trauma
Temperature
Ionising radiation- DNA damage
Electric shock-burn

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7
Q

How chemical & drugs may cause cell injury?

A

Osmotic disturbance - excess glucose
Poisons - cyanide
Occupational hazards - asbestos
Alcohol, smoking, drug abus

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8
Q

How immunological reaction may cause cell injury?

A

Anaphylaxis - tp1 HS
Auto-immune reactions (tp 2, antibodies directed towards host antigens, tp 3 – antigen-antibody complex)
Damage mediated by inflammation

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9
Q

How Nutrition imbalance can cause cell injury?

A

Inadequate:
Specific- rickets, scurvy
Generalised- Anorexia

Excessive:
Specific - Hpervitaminosis
Generalised - Obesity

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10
Q

How Genetic defects may cause cell injury?

A

Sickle cell anaemia
Inborn error of metabolism
Cancer

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11
Q

Injury to cells causes disruption to:

A
  • Aerobic respiration/ATP synthesis (Mitochondrial damage)
  • Plasma membrane integrity
  • Enzyme & structural protein synthesis
  • DNA maintenance
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12
Q

What happen when cells present as cloudy swelling?

A
  • Cells incapable of maintaining ionic & fluid homeostasis
  • ATP dependant pumps lose function → Influx of Na & H20
  • Build up of intracellular metabolites
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13
Q

What happen when cell present as fatty changes?

A
  • Lipid vacuole accumulation → via fatty acid metabolism disruption
  • Triglycerides cannot be released from cell
  • Toxic & Hypoxic injury - Alcohol abuse, obesity, diabetes
  • Commonly associated with enlarged liver & spleen
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14
Q

What is necrosis?

A

Cell death (Usually from pathological consequences)

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15
Q

What are the nuclear changes in necrosis?

A
  • Pyknosis - Nucleus shrinks (Darker stain)
  • Karyorrhexis - Nucleus fragments
  • Karyolysis - Dissolution of Nuclear components
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16
Q

What are the cytoplasmic changes in necrosis?

A
  • Appears paler & swollen
  • Sometime more eosinophilic → Increased denaturation of cytoplasmic enzymes /protein
17
Q

Mention types of necrosis?

A

Coagulative necrosis
Liquefactive necrosis
Caseous necrosis
Gangrenous necrosis
Fat necrosis
Fibrinoid necrosis

18
Q

What is infarct?

A

Localised area of coagulative necrosis

19
Q

What type of necrosis it appearance like cheese?

A

Caseous necrosis

20
Q

What type of necrosis seen in immune reactions in blood vessels?

A

Fibrinoid necrosis

21
Q

What type of necrosis is characterize by release of lipases, formation of fatty acids, saponification ?

A

Fat necrosis

22
Q

What are the effects of necrosis?

A

Loss of function - Organs/tissues
Inflammation - Phagocytosis and clearance of necrotic tissue
Scar tissue generation - Repair
Calcium salt deposition - If necrotic remains are still present

23
Q

What is Apoptosis?

A

Genetically programmed cell death

24
Q

What are the Apoptotic triggers?

A

Hypoxia/Ischaemia
Viral infection - mediated by CD8+ (Induced apoptosis)
DNA damage - mediated by p53 (Tumour-suppressor gene)
Caspases - active enzymes that trigger apoptosis

25
Q

What are the physiological functions/roles of apoptosis?

A

Embryogenesis - Cell population deletion
Hormone mediated involution - Uterus, breast, ovary
Population maintenance - epithelium
Inflammatory cell deletion - once threat is resolved
Negative selection of T cells - In thymus

26
Q

What too much and little apoptosis cause?

A

Too much apoptosis= degenerative diseases
Too little apoptosis= cancer

27
Q

What is Intracellular accumulation?

A
  • Excessive normal cellular constituents → Water, lipid, glycogen
  • Abnormal endogenous/exogenous material → Carbon, Silica, metabolites, cholesterol
28
Q

What is cholesterol accumulation?

A
  • Atherosclerosis - build up in smooth muscle of blood vessel walls
  • Fatty necrosis
  • Presence of foam cells - Where macrophages ingest lipid
29
Q

What is Amyloid?

A
  • Fibral protein deposition → due to increased pathological production
  • Deposited mostly on basement membranes of tissue/organs
30
Q

Mention types of Amyloid:

A
  • AL amyloid - Amyloid light chain → From light chain immunoglobulins from plasma cells
  • AA amyloid - Amyloid associated → protein derived from liver
  • Aβ amyloid - Alzheimer’s disease
31
Q

Mention Amyloid Stimuli?

A
  • Chronic inflammation
  • Multiple myeloma
  • Ageing
  • Drug abuse
32
Q

What is Pathological Pigmentation?

A

Pigmented substance build up in cytoplasm

33
Q

Mention Endogenous pigmentation

A

Melanin
Bilirubin
Hameosiderin-localised bruising
Lipofuscin-cellular lipid breakdown products

34
Q

Mention Exogenous pigmentation

A

Carbon deposition
Tattoos
Heavy metal salts - Lead
Intravascular drug use

35
Q

Pathological Calcification

A

Dystrophic calcification → Calcium phosphate deposits in necrotic tissues

Metastatic calcification → deposits in vital tissue due to 📈 serum calcium

36
Q

What causes raised calcium levels?

A
  • Increased PTH activity → Hyperparathyroidism
  • Bone tissue destruction → via bone metastasis (Leukaemia)
  • Vitamin D excess
  • Renal failure - secondary hyperparathyroidism