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Cell injury Flashcards

1
Q

Severe changes in the environment lead to

A

cell adaptation, injury or cell death.

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2
Q

Degree of injury depends on:

A

Type of injury

Severity of injury

Duration of injury

Type of tissue

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3
Q

What can causes injury to a cell?

A
  • Hypoxia
  • Toxins
  • Physical agents
    • Direct trauma
    • Extreme temp
    • Changes in pressure
    • Electric currents
    • Radiation
    • Microorganisms
    • Immune mechanism
    • Dietary insufficiency and deficiency’s, dietary excess
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4
Q

Cell components most susceptible to injury

A

1. Cell membranes

  • Plasma membrane
  • Organelle membrane

2. Nucleus

  • DNA

3. Proteins

  • Structural (enzymes)

5. Mitochondria (oxidative phosphorylation)

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5
Q

How does the immune system damage the body’s cells?

A

Hypersensivity reactions

Autoimmune reactions

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6
Q

Hypersensivity reactions

A

host tissue is injured secondary to an overly vigorous immune reaction e.g. urticaria (hives)

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7
Q

Autoimmune reactions

A

immune system fails to distinguish self from non-self e.g. Graves disease of thyroid

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8
Q

hypoxia is due to

A

ischaemia

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9
Q

ischaemia

A

is insufficient blood flow to provide adequate oxygenation.

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10
Q

causes of hypoxia

A

hypoxaemic hypoxia

anaemic hypoxia

ischaemic hypoxia

histotoxic hypoxia

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11
Q

Hypoxaemic hypoxia

A

-arterial content of oxygen is low

  • Reduced inspired pO2 at altitude
  • Reduced absorption secondary to lung disease
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12
Q

Anaemic hypoxia

A

decreased ability of haemoglobin to carry oxygen

  1. Anaemia
  2. CO poisoning
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13
Q

Ischaemic hypoxia

A

interruption to blood supply

  1. Blockage of a vessel
  2. Heart failure
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14
Q

Histotoxic hypoxia

A

inability to utilise oxygen in cells due to disabled oxidative phosphorylation enzymes

  1. Cyanide poisoning
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15
Q

hypoxia can be

A

reversible or irreversible (if prolonged)

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16
Q
A
  1. Ischaemia causes a reduction in oxidative phos in the mitochondria
  2. Less ATP produced
  3. Reduced Na pump = influx of calcium, H2O and Na+, effluent of K+
    1. cellular swelling
    2. Loss of microvilli
    3. Bless
    4. ER swelling
    5. Myelin figures
  4. Increased glycolysis
    1. decreased pH (cli]umping of nuclear chromatin)
    2. Decreased glycogen 5) other affects
    3. detachment of ribosomes
    4. Decreased protein synthesis
    5. Lipid depositor
  5. Decreased protein synthesis
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17
Q

prolonged hypoxia is

A

irreversible

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18
Q

characteristics of injured/dying cell

A
  • cytoplasmic changes
  • nuclear changes
  • abnormal cellular accumulations
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19
Q

blebs

generalised swelling

A
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20
Q

nuclear changes

A
  • abnormal clumping of nuclear chromatin
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21
Q

Abnormal cellular accumulations

A
  • dispersion of ribosomes, swelling of mitochondria and ER
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22
Q

alive vs injured vs dead cells

A
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23
Q

Pyknosis

A

is the irreversible condensation of chromatin in the nucleus of a cell undergoing necrosis or apoptosis. It is followed by karyorrhexis, or fragmentation of the nucleus.

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24
Q

Karyorrhexis

A

is the destructive fragmentation of the nucleus of a dying cell whereby its chromatin is distributed irregularly throughout the cytoplasm.

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25
karyolysis
dissolution of a cell nucleus, especially during mitosis.
26
other causes of cell injury
extreme cold and free radicals
27
definition of a free radicale
Single unpaired electron in an outer orbit- unstable configuration hence reacts with other molecules--\>producing further free radicals
28
examples of reactive oxyen species
• OH• (hydroxyl) - the most dangerous * O2- (superoxide) * H2O2 (hydrogen peroxide)
29
30
Exogenous factors which increase formation of free radicals
* Smoking * Ionising radiation * Air pollution * UV light * Inflammation * Metabolism
31
formation of free radical
* **Normal metabolic reactions** e.g. oxidative phosphorylation * **Inflammation**- oxidative burst of neutrophils * **Radiation** * **Contact with unbound metals** within the body: iron (by Fenton reaction) and copper * Free radical damage occurs in hemochromatosis and Wilsons disease * **Drugs and chemicals** e.g. the liver during metabolism of paracetamol or carbon tetrachloride by P450 system
32
how do free radicals injure cells?
Most important targets are lipids in cell membranes Also oxidise proteins, carbohydrates and DNA
33
how do free radicals damage lipids in the cell membrane
* Cause lipid peroxidation * This leads to generation of further free radicals --\> autocatalytic chain reaction
34
ROS oxidise proteins, carbohydrates and DNA
These molecules become bent out of shape, broken or cross-linked Mutagenic and therefore carcinogenic
35
how does the body control free radicals?
**1. Anti-oxidant scavengers** * Donate electrons to the free radical * e.g. Vitamin A, C and E **2. Metal carrier and storage proteins** * transferrin, ceruloplasmin --\> sequester ion and copper **3. Enzymes that neutralise free radicals** - superoxide dismutase - catalase **- glutathione peroxidase (GSH)**
36
abnormal cellular accumulations
When metabolic processes become deranged: * Sublethal or chronic injury * Can be reversible * Can be harmless or toxic * Derived from: * Cells own metabolism * Extracellular space e.g. spilled blood * Outer environment e.g. dust
37
Mechanisms of intracellular accumulations
* Abnormal metabolism * Alterations in protein folding and transport * Deficiency of critical enzymes * Inability to degrade phagocytosed particles
38
What can accumulate?
* Fluid * Lipids * CHO * Proteins * Pigment
39
(1) Fluid accumulation in cells
* **Hydropic swelling** * Occurs when energy supplies are cut off e.g. hypoxia * Indicates severe cellular distress * **Na+ and water flood into cell**
40
where is fluid accumulation in cells particularly dangerous
Particular problem in the brain
41
(2) Lipid accumulation in cells
Steatosis (accumulation of triglycerides)
42
where is lipid accumulation in cells often seen
in the liver (major organ of fat metabolism) - if mild asymptomatic
43
causes of lipid accumulation
* Alcohol * Diabetes mellitus * Obesity * Toxins (carbon tetrachloride
44
what does steatosis look like?
45
(3) Protein accumulation in cells is seen as
eosinophilic droplets or aggregations in the cytoplasm
46
examples of when protein accumulates in cells
alcohol liver disease alpha-1-antitrypsin deficiency
47
alcohol liver disease
Mallorys hyaline (damaged keratin filaments)
48
α1-antitrypsin deficiency
* Liver produces incorrectly folded α1-antitrypsin protein (a protease inhibitor) * Cannot be packaged by ER, accumulates within ER and is not secreted * Systemic deficiency – proteases in lung act unchecked resulting in emphysema
49
(4) Exogenous and endogenous pigment accumulation in cells
* Carbon/coal dust/ soot- urban air pollutant * Inhaled and phagocytosed. By alveolar macrophages * Anthracosis and blackened peribronchial lymph nodes * Usually harmless, unless in large amounts * Fibrosis * And emphysema (coal workers pneumoconiosis)
50
Other examples of exogenous
* Tattooing- pigments pricked into skin * Phagocytosed by macrophages in **dermis and remains there** * Some pigment will reach draining lymph nodes
51
52
endogenous pigment accumulation in cells
hemosiderin
53
hemosiderin
* Iron storage molecule * Derived from Hb- yellow/ brown * Forms when there is systemic or local excess of iron e.g. bruise * With systemic overload of iron, hemosiderin is deposited in many organs = hemosiderosis * Seen in haemolytic anaemias, blood transfusions and hereditary hemochromatosis
54
Hereditary haemochromatosis
* Genetically inherited disorder - results in increased intestinal absorption of dietary iron * Iron is deposited in skin, liver, pancreas, heart and endocrine organs - often associated with scarring in liver (cirrhosis) and pancreas.
55
symptoms of Hereditary haemochromatosis
* liver damage * heart dysfunction * multiple endocrine failures- especially of the pancreas. * was called 'bronze diabetes'
56
Treatment of Hereditary haemochromatosis
is repeated bleeding
57
jaundice
Accumulation of bilirubin – bright yellow Breakdown product of heme, stacks of broken porphyrin rings Formed in all cells of body (cytochromes contain heme) but must be eliminated in bile
58
jaundice is the
accumulation of bilirubin- bright yellow
59
bilirubin is the
product of heme- stacks of broken prophyrin rings
60
haem is taken from tissues by
albumin to the liver- iron is recycled and haem becomes bilirubin. bilirubin becomes conjugated with glucoronic acid to become bile
61
62
unconjugated bilirubin transported in the blood bound
to albumin - when in excess can cause jaundice
63
When membranes are leaky can molecules leak out as well??
Yes- can have both local and systemic effects * local inflammation * may have general toxic effects on body * May appear in high conc in blood and can aid in diagnosis
64
examples of molecules which can leak out of the cell if damaaged
* Enzymes * CK * AST * Troponin * Myoglobin * Rhabdomyolysis * Potassium
65
pathological calcification
* Abnormal deposition of calcium salts within tissues * Can be localised (dystrophic) or generalised (metastic)
66
dystrophic calcification is much more
common than metastatic
67
where does dystrophic calcification occur?
* in area of dying tissue * atherosclerotic plaques * ageing of heart valves * in tuberculus lymph nodes * some malignancies
68
causes of dystrophic calcification
* No abnormality in calcium metabolism- or serum calcium or phosphate conc * Local change/disturbance * Favours nucleation of hydroxyapatite crystals
69
dystrophic calcification can cause
organ dysfunction e.g. atherosclerosis or calcified heart valve
70
Causes of metastatic calcification
* Due to hypercalcaemia secondary to disturbances in calcium metabolism * Hydroxyapatite crystals are deposited in normal tissues throughout the body * Usually asymptomatic but it can be lethal * Can regress if the cause of hypercalcaemia is corrected
71
causes of hypercalcaemia
* Increased secretion of parathyroid hormone (PTH) resulting. * Destruction of bone tissue
72
Increased secretion of parathyroid hormone (PTH) resulting. In bone resorption:
* Primary- due to parathyroid hyperplasia or tumour * Secondary- due to renal failure and retention of phosphate * Ectopic- secretion of PTH related protein by malignant tumours (carcinoma in lungs)
73
destruction of the bones
* Primary tumours of bone marrow, e.g., leukaemia, multiple myeloma * Diffuse skeletal metastases * Paget’s disease of bone – when accelerated bone turnover occurs * Immobilisation

Pathological processes (19 decks)

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