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Pathology > Cell Injury/Apoptosis/Necrosis > Flashcards

Cell Injury/Apoptosis/Necrosis Flashcards

1
Q

Most common cause of cell injury?

A

Hypoxia

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2
Q

4 causes of hypoxia?

A

Hypoxaemic - eg altitude
Anaemic - Reduces O2 carrying capabilities
Ischaemic - e.g. blockage atherosclerosis
Histocytic - Problem with oxidative phosphorylation in cell e.g. cyanide poisoning

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3
Q

Give an example of a cell that is sensitive to hypoxia, compared to one that can withstand effects of hypoxia for longer?

A

Neurones - sensitive

Fibroblasts - can last hours

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4
Q

Which 4 components of the cell (e.g. organelles) are most susceptible to hypoxia?

A

Cell membranes, nucleus, proteins, mitochondria

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5
Q

Which 2 ways can the immune system damage cells?

A

Hypersensitivity - e.g. vigorous immune response - hives etc

Autoimmune - recognise self as foreign and destroy

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6
Q

3 cellular effects of hypoxia that is short-lived/reversible?

A

1) Mitochondria use up remaining O2 so oxidative phosphorylation slows down - ATP reduces (less made) therefore reduced NaKATPase - means Na and H2O enters cell - Ca2+ follows in (Na+ out) - Cell swelling
5) Anaerobic respiration causes pH drop
6) Ribosome detachment as held with ATP - disruption of protein synthesis

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7
Q

Which two substances in the body are very metabolically active and need to be controlled?

A

Iron and Ca2+

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8
Q

3 cellular effects of prolonged/irreversible hypoxia?

A

1) Huge influx of Ca2+
2) Enzyme leakage - cellular destruction
3) Disruption to plasma membrane

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9
Q

What is H202?

A

Hydrogen peroxide - is a reactive oxygen species

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10
Q

What are free radicals needed for in the cell?

A

1) Oxidative phosphorylation

2) Neutrophil oxidative burst

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11
Q

What is the major way free radicals injure cells?

A

Via lipid peroxidation - cell membrane damage.

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12
Q

What are heat shock proteins?

A

Proteins that are produced by the cell in response to stress (e.g. heat/injury). Have a role in repair e.g. misfolding of proteins to help maintain cell viability

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13
Q

5 causes of free radical formation? (exo and endo)

A

1) Oxidative phosphorylation
2) Neutrophil oxidative burst - Inflammation
3) Contact with unbound metals - iron/copper
4) Drug metabolism in liver - e.g. paracetamol
5) Radiation e.g. UV

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14
Q

Is a pale, swollen cell likely to be injured or dead?

A

Injured

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15
Q

What is pyknosis?

A

Pink - takes up Eosin due to clumped chromatin, nucleus appears small - shrinks

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16
Q

What is karyolysis?

A

Nucleus dissolves due to enzymes

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17
Q

What is karyohexis?

A

Nucleus fragments

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18
Q

What are blebs? How do they occur?

A

Swellings in the membrane due to cell injury - Ca2+ activated proteases begin to break down cytoskeleton

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19
Q

8 cellular signs (on EM) of cell damage that is reversible?

A

1) Blebs
2) Autophagy of lysosomes
3) Cell swelling
4) Chromatin clumping
5) Aggregation of intramembranous particles
6) ER swelling
7) Dispersion of ribosomes
8) Small densities in cell

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20
Q

7 cellular signs (on EM) of cell damage that is now irreversible?

A

1) Lysosome autolysis
2) Nuclear - pyknosis, karyolysis or karyohexis
3) Large densities in cell
4) Myelin figures (fats collect under cell surface)
5) Mitochondrial swelling (H2O now goes in)
6) Lysis of ER (due to swelling)
7) Defects in cell membrane

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21
Q

Is it easier to determine if a cell is dead by looking at structure or function?

A

Function

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22
Q

Which type of necrosis is by protein denaturation?

A

Coagulative

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23
Q

Which type of necrosis is by enzyme release?

A

Liquefactive

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24
Q

What is caseous necrosis most commonly seen in?

A

TB

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25
Q

Where (2) might you see fat necrosis in the body?

A

Breast/Pancreas

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26
Q

What is reperfusion injury? What are 3 possible causes?

A

Damage may be worse after reperfusing an injured by not necrosed tissue. Could be due to 1) increased formation of free radicals with return of O2 2) Increased blood flow bringing inflammation cells e.g. neutrophils—> worsens area of damage 3) Activation of complement system by delivery of complement proteins

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27
Q

What important things move out of the cell when a cell membrane becomes leaky? What effects can this have on the body?

A

1) K+ leaks out - cardiac arrhythmias
2) Enzymes leak out - e.g. troponin can measure
3) Myoglobin leaks out - blocks glomeruli in the kidney causing renal failure - rhabdomyolysis

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28
Q

What is apoptosis

A

Cell death with shrinkage and programmed DNA and protein degradation via intracellular activation of enzymes

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29
Q

Which type of cell death begins with cell swelling, an which with cell shrinkage?

A

Necrosis - swelling

Apoptosis - shrinkage

30
Q

Is Apoptosis active or passive?

A

Active

31
Q

Is Apoptosis always pathological?

A

No can be physiological e.g. embryo fingers

32
Q

Is Apoptosis slow or quick?

A

Quick - few hours

33
Q

Which method of cell death disrupts cell membrane - apoptosis or necrosis?

A

Necrosis - in apoptosis membrane integrity is maintained

34
Q

Are lysosomal enzymes involved in apoptosis necrosis or both?

A

Necrosis

35
Q

When might apoptosis occur (3)?

A

When there is a danger to cell e.g. DNA damage, virus/neoplastic, bone marrow graft

36
Q

Do cytotoxic T cells cause apoptosis? If so when?

A

Yes e.g. viruses or neoplastic cells

37
Q

What is graft versus host disease?

A

If someone has a bone marrow transplant e.g. in cancers, new WBC produced by bone marrow can recognise host as foreign and begin to apoptose cells e.g. in skin, rectum, bowel (particularly prone areas)

38
Q

Which method of cell death wipes out a larger area of tissue and which a smaller area?

A

Necrosis - large

Apoptosis - single cell

39
Q

5 cellular effects (visible on EM) characteristic of apoptosis?

A

Cell shrinkage
Chromatin condensation
Karyorexis (more common in apoptosis than necrosis)
Budding - break off and usually have some organelles in e.g. nucleus/mitochondria
Apoptotic bodies - formed from budding with organelle in

40
Q

What are caspases role in apoptosis?

A

They control apoptosis - cause DNA and protein cleavage

41
Q

What two pathways lead to apoptosis?

A

Intrinsic and extrinsic

42
Q

What happens in the intrinsic apoptotic pathway? What is the role of p53 and cytochrome C?

A

Intracellular mechanism most commonly due to DNA damage but also removal of growth hormones. p53 protein activated and results in the outer mitochondrial membrane becoming leaky. Cytochrome C is released from mitochondria and causes activation of caspases

43
Q

What happens in the extrinsic apoptotic pathway? What is the role of TNF-alpha?

A

Usually extrinsic trigger e.g. immune response to antigen/tumour cell. One signal is TNF-alpha that is secreted by T killer cells, and binds to ‘death receptors’ on the cell activating caspases

44
Q

Apoptotic bodies are phagocytosed - what allows them to be recognised for phagocytosis? Is this inflammatory?

A

Proteins on their membrane. There is no inflammation unlike necrosis

45
Q

Is necrosis ever physiological?

A

No always pathological

46
Q

Intracellular accumulations can occur in cell damage - what 5 main groups of substances accumulate? Why would something accumulate in the cell?

A

Proteins - keratin/alpha-1 antitrypsin
Carbohydrates - ?
Lipids - steatosis in liver/cholesterol
Water and electrolytes - loss of NaKATPase so Na and therefore H2O in.
‘Pigments’ - bilirubin/carbon/haemosiderin

If it can’t be metabolised, something extracellular e.g. blood, outer environment e.g. dust

47
Q

Why is hydropic swelling? When does it occur? Why is this a particular problem in the brain?

A

Swelling due to fluid accumulating in cells - sign of severe cell injury, Na+ and therefore H2O into cell e.g. in hypoxia. Problem in brain as skull prevents expansion - structures get compressed and ischaemic - can be fatal.

48
Q

What is Steatosis? Why does this happen particularly in the liver? Is this reversible? Is this fatty liver?

A

Steatosis is lipid accumulation (triglycerides) - happens in liver as liver a major site of lipid metabolism. There is ribosomal detachment meaning liver hepatocytes can’t produce lipoproteins meaning the lipids accumulate in the cells. Can be reversible e.g. after alcohol in around 10 days, obesity, diabetes, toxins e.g. carbon tetrachloride. Yes fatty liver.

49
Q

What happens to the nucleus in steatosis and why?

A

Gets pushed to the periphery due to fat accumulation in hepatocytes

50
Q

What effect does carbon tetrachloride have on hepatocytes?

A

Causes lipid accumulation - steatosis

51
Q

Why does cholesterol accumulate in cells and why?

A

If you have excess it will accumulate in cells as cannot be broken down, is insoluble and can only be eliminated by the liver. Will accumulate in SMCs and macrophages - foam cells. Causes fatty streaks in arteries/ may accumulate in skin called xanthomas

52
Q

What is a xanthoma and why does it occur?

A

Cholesterol accumulation in the skin e.g. in hereditary hyperlipidaemia.

53
Q

If you saw eosinophilic droplets or aggregations in cytoplasm what kind of substance accumulation would you be thinking? When would this occur?

A

Protein.

54
Q

Give examples of two diseases where proteins accumulate in cells

A

1) Alcoholic liver disease- Mallory’s hyaline (damaged keratin filaments)
2) Alpha-1 antitrypsin deficiency - alpha-1 antitrypsin protein deficient and cannot be folded properly so is therefore not secreted. Causes cirrhosis of liver and emphysema

55
Q

How does alpha-1 antitrypsin deficiency lead to emphysema?

A

Proteases in lung act uninhibited and therefore destroy alveoli

56
Q

What is a common pigment that accumulates in the lung? In what cells does pigment accumulate? What is this called? Is this harmful?

A

Carbon/soot etc from smoking/air pollutant. Accumulates in alveolar macrophages along peribronchial lymph nodes. Called anthracosis. Normally harmless but harmful if in large quantities - coal workers pneumoconiosis

57
Q

What is haemosiderin? What does it often form after?

A

An iron storage molecule within cells, derived from Hb. Normally forms after bleeding - breakdown of Hb and uptake of RBCs by macrophages. Haemosiderin most commonly found in macrophages

58
Q

What is haemosiderosis? What conditions is in more commonly seen (3)?

A

Build of haemosiderin that then deposits in organs.
See in haemolytic anaemia
Blood transfusions
Hereditary haemochromatosis

59
Q

What is hereditary haemochromatosis? What happens and what is the treatment?

A

Genetic condition resulting in excess absorption of iron from the intestine. Results in iron deposits in organs e.g. skin, pancreas, liver, heart. Skin looks brown and can cause liver cirrhosis and pancreatic insufficiency (diabetes). Treatment is repeated bleeding to remove excess iron.

60
Q

What is bilirubin? How is it formed? Is it only formed in the liver? How is it excreted?

A

Bilirubin is a yellow pigmented compound that is formed during the breakdown of heme molecules (e.g. from Hb) - broken down porphyrin rings. No formed in all cells - travels with albumin to the liver where it can be conjugated and excreted in bile - via bile duct to GI - then either in faeces, or via blood to kidney then in urine.

61
Q

What is icterus?

A

Sclera jaundice - first place to usually look for jaundice

62
Q

What accumulates in jaundice and where? Why is it a problem?

A

Bilirubin - in macrophages or in tissues extracellularly. BIlibrubin can be toxic to brain

63
Q

What is metastatic vs dystrophic calcification? What is being deposited in calcification?

A

Dystrophic - local calcification in dying tissue e.g. in atherosclerotic plaques, ageing/damaged heart valves, some malignancies e.g. breast (can be picked up with mammogram)

Metastatic - is body wide calcium deposition in cells. Calcium salts are being deposited

64
Q

Is there a change in calcium metabolism or serum concentration in dystrophic calcification? What happens? Does this affect organ function?

A

No change - is a local disturbance that causes nucleation of of hydroxyapatite crystals (calcium salts). Can cause organ dysfunction e.g. atherosclerosis/heart valve calcification can affect function

65
Q

What happens in metastatic calcification? Is there a change in Ca metabolism or serum concentration? Is this dangerous? Can it be reversed?

A

Yes due to hypercalcaemia secondary to disturbances in calcium metabolism. Hydroxyapatite crystals are deposited in normal cells throughout the body - usually asymptomatic but can be fatal - can be reversed if cause of hypercalcaemia is reversed.

66
Q

Two causes of hypercalcaemia?

A

Increased parathyroid hormone - so increased bone resorption e.g. parathyroid tumour

Increased destruction of bone e.g. in bone marrow tumours

67
Q

Myeloma, Pagets disease, immobility and malignancy can all cause what? Why?

A

Hypercalcaemia. Myeloma and malignancy - destruction of bone. Pagets leads to increased bone turnover. Immobility leads to loss of stimulus for bone laying down new bone but do have stimulus for bone resorption

68
Q

What is replicative senescence?

A

Every cell has certain number of replications and after this won’t replicate any more. It is related to the length of chromosome - telomeres.

69
Q

Do any cells ‘live forever’? Why?

A

Germ cells and cancer cells - have telomerase

70
Q

Define histiocytic hypoxia vs hypoxaemic hypoxia?

A

Histiocytic - reduced ability for cells to take up and utilise O2 e.g. in CO poisoning

Hypoxaemic hypoxia - Insufficient oxygen supplied to lungs e.g. reduction in PPO2 at altitude.

71
Q

Name 4 cellular changes in reversible cell injury

A

1) Cell swelling and organelle swelling (mito/lysosomes etc)
2) Ribosomal detachment
3) Blebbing
4) Nuclear/chromatin clumping

72
Q

Name 4 cellular changes of irreversible cell injury

A

1) Membrane damage
2) Nuclear changes - Pyknosis/Karyorrhexis, Karyolysis
3) Lysosomal swelling and bursting (and other organelles e.g. ER)
4) Myelin figures (fat collections under membrane)

Pathology (13 decks)

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