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Semester 2 - Mechanism of Disease > MoD S1 - Cell injury > Flashcards

MoD S1 - Cell injury Flashcards

1
Q

List the main causes of cell injury

A
  • Hypoxia
  • Micro-organisms
  • Immune response
  • Physical agents
  • Chemical agents
  • Dietary insufficiency or excess
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2
Q

What is hypoxia?

A

Oxygen deprivation resulting in decreased aerobic oxidative phosphorylation

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3
Q

How do different cells respond to hypoxia?

A

Fibroblasts can survive for hours whereas neurones can tolerate only minutes before suffering injury and subsequent death

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4
Q

What are the causes of hypoxia?

A

Hypoxaemic‐ arteriole oxygen content is low

Anaemic‐ decreased ability of haemoglobin to carry oxygen

Ischaemic‐ interruption of oxygenated blood supply

Histiocytic‐ cannot use oxygen in cells due to disabled oxidative phosphorylation enzymes

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5
Q

How can immune mechanisms result in cell injury?

A
  • Hypersensitivity reactions where host tissue is damaged secondary to vigorous immune response
  • Autoimmune reactions where immune system fails to distinguish self from non‐self
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6
Q

What are the main targets for cell injury?

A

Membrane, Nucleus, Mitochondria, Proteins (both structural and enzymes)

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7
Q

Outline the steps of hypoxic cell injury

A
  • Cell deprived of oxygen
  • Mitochondrial ATP production stops
  • ATP‐driven membrane ionic pump stops
  • Sodium and water seep into cell
  • Cell swells and plasma membrane is stretched
  • Glycolysis enables cell to survive for a while
  • Cell initiates heat shock response
  • pH drops as lactate accumulates from glycolytic ATP production
  • Calcium enters cell (changes now become irreversible)
  • Calcium activates phospholipases, endonucleases, proteases and ATPase
  • ER and organelles swell
  • Enzymes leak out of lysosomes and attack cytoplasmic components
  • Cell membrane is damaged and starts to show blabbing
  • Cell dies
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8
Q

What is blebbing in cell injury?

A

Cell membrane separates from the cytoskeleton

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9
Q

What is ischemic reperfusion injury?

A

Blood flow returned to tissue which isn’t yet necrotic causing excess free radical production, increased complement proteins and activation of the complement pathway and increased neutrophils causing inflammation

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10
Q

What is chemical injury?

A

Chemical binds to a cell component e.g. cyanide binding to cytochrome oxygenase blocking oxidative phosphorylation

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11
Q

When are free radicals produced in cells?

A
  • Excess oxygen
  • Cellular aging
  • Ischemic‐reperfusion injury
  • Chemical and radiation injury
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12
Q

How are hydroxyl radicals produced in cells?

A

Lysis of water, Fenton and Harber‐Weis reactions

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13
Q

What are the three main mechanisms of defence against free radicals within cells?

A

Enzymes‐ superoxide dismutase, catalase and peroxidase

Free radical scavengers‐ vitamins A, C and E and glutathione

Storage proteins‐ sequester transition metals in the extra cellular matrix

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14
Q

What test can be used to identify cell death?

A
  • Dye exclusion test

- Based on functional not morphological criteria

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15
Q

What morphological changes can be seen in injured cells under a light microscope?

A

Cytoplasmic:
● reduced pink staining due water moving in (reversible)
● become intensely eosinophilic as proteins aggregate together (irreversible)

Nuclear:
● chromatin clumping (reversible)
● pyknosis, karryohexis, karryolysis (irreversible)

Abnormal cellular accumulations

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16
Q

What reversible changes to injured cells can be seen under an electron microscope?

A
  • Swelling due to Na/K pump failure
  • Cytoplasmic blebs
  • Clumped chromatin due to changes in pH
  • Ribosomes detach from ER due to lack of ATP
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17
Q

What irreversible changes to injured cells can be seen under an electron microscope?

A
  • Increased cell swelling
  • Amorphous densities in swollen mitochondria
  • Swelling and rupture of lysosomes
  • Lysis of ER membrane
  • Nuclear changes‐ pyknosis, karryohexis, karryolysis
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18
Q

Define oncosis

A

Cell death with swelling, it is the spectrum of changes that occur prior to death in cells injured by hypoxia

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19
Q

Define apoptosis

A

Cell death with shrinkage, induced by a regulated intracellular programme where a cell activates enzymes that degrade its own and DNA and proteins

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20
Q

Outline the main steps in the initiation of apoptosis

A

Intrinsic activation‐ increased permeability of mitochondria, release of cytochrome C, binds to caspase 9 and APAF‐ 1 to form an apoptosome, activation of various downstream caspases

Extrinsic activations‐ death ligands such as TRAIL bind to receptors such as TRAIL‐R and activate caspases independent of mitochondria

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21
Q

Outline the main steps of the execution stage of apoptosis

A

Caspases are the effector molecules of apoptosis and when activated are proteases that break down the cytoskeleton and initiate degradation of DNA

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22
Q

Outline the main steps of the degradation stage of apoptosis

A

Cell breaks down to form membrane bound fragments called apoptotic bodies which have antigens present on their surface, marking them for phagocytosis

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23
Q

List the important apoptotic molecules

A
  • Cytochrome C, caspase 9 and APAF‐1
  • Bcl‐2
  • p53
  • Caspases
  • Death Ligands e.g. TRAIL
24
Q

Define necrosis

A

In living organisms the morphological changes that occur after a cell has been dead for 4‐24 hours

25
Q

What are the four types of necrosis?

A

Liquifactive, coagulative, caseous, fat

26
Q

Describe liquifactive necrosis

A

Active degradation exceeds protein denaturation leading to enzymatic digestion to form a viscous mass

27
Q

When does liquifactive necrosis occur?

A

Bacterial infections due to increased number of neutrophils

Fragile tissues such as the brain which lack a strong collagenous support

28
Q

Describe coagulative necrosis

A

Denaturation of proteins dominates over release of active proteases so dead tissue has solid consistency

Ghost outlines form

29
Q

Describe caseous necrosis

A

Resembles cheese, characterised by amorphous, structureless debris

30
Q

What infection is caseous necrosis most commonly associated with?

A

Tuberculosis

31
Q

What type of inflammation is caseous necrosis associated with?

A

Granulomatous

32
Q

Describe fat necrosis and its appearance

A

Destruction of adipose tissue

Free fatty acids released react with calcium ions to form chalky deposits

33
Q

What are the main causes of fat necrosis?

A

Pancreatitis, direct trauma to fatty tissue such as breast

34
Q

What is gangrene?

A

Clinical term describing necrosis visible to the naked eye

Gangrenous tissue is dead and cannot be recovered

35
Q

What are the two types of gangrene?

A

Wet - liquifactive necrosis, exposed to bacteria, often leads to septicaemia

Dry‐ coagulative necrosis, exposed to air

36
Q

List the molecules released in cell injury

A

Potassium‐ dying cell is referred to as potassium bomb e.g. MI, massive necrosis or tumour lysis syndrome

Enzymes‐ indicate the organ involved, extent, timing and evolution of the damage with smallest molecular weight enzymes being released first

Myoglobin‐ released from cardiac or skeletal muscle causing rhabdomyolysis which plugs renal tubules casing renal failure

37
Q

When do abnormal cellular accumulations occur?

A

Sub‐lethal or chronic injury when metabolic processes become deranged

38
Q

When does fluid accumulate in cells?

A

Due to osmotic disturbance when energy supply to cell cut off e.g. ischaemia

39
Q

What are the different types of lipid accumulation in cells?

A

Steatosis‐ accumulation of triglycerides particularly in the liver, often due to obesity, alcohol, diabetes and toxins

Phospholipids‐ disrupted cell membranes from myelin figures

Cholesterol‐ builds up in smooth muscle cells and macrophages in atherosclerotic plaques creating foam cells

40
Q

Give an example of an exogenous pigment

A

Carbon‐ urban air pollutant, inhaled and phagocytosed, blackens lungs and can cause lungs to be fibrotic or emphysematous

Tattoo‐ phagocytosed in dermis where it remains indifenitely, may build up in lymph nodes

41
Q

What is lipofuscin?

A

Endogenous age pigment, brown lipid

42
Q

What is haemosiderin?

A

Endogenous yellow/brown iron storage molecule which forms due to a systematic or local excess of iron

43
Q

Describe the structure of bilirubin

A

Stack of opened porphyrin rings that have lost their iron

44
Q

What are the two types of protein accumulation in injured cells?

A

Mallory’s hyaline‐ keratin filaments seen in damaged hepatocytes in alcoholic liver disease

Alpha1‐antitrypsin deficiency‐ misfolded protein cannot be packaged in ER so is not released by liver, means that proteases in lungs go unchecked resulting in emphysema

45
Q

Define infarction

A

Cause of necrosis, area of tissue death by obstruction of a tissues blood supply

46
Q

What are the possible causes of infarction?

A

Thromobsis, embolism, twisted blood vessel or external compression of blood vessel

47
Q

What is a white infarct and how is it caused?

A

Occurs in solid organs after occlusion of an end artery

Appears as coagulative necrosis

48
Q

What tissues may suffer a white infarct?

A

Heart, kidneys, spleen

49
Q

What is a red infarct?

A

Extensive haemorrhage into dead tissue

50
Q

What are the possible causes of a red infarct?

A
  • Dual blood supply
  • Multiple anastomoses
  • High venous pressure
  • Loose tissue with poor stromal support for capillaries
  • Previous congestion
51
Q

What is pathological calcification?

A

Abnormal deposition of calcium salts in tissues

52
Q

What are the two types of calcification and how do they differ?

A

Dystrophic‐ occurs in local areas of dying tissue, no abnormality in calcium metabolism

Metastatic‐ body wide disturbance secondary to hypercalcaemia due to disturbance in calcium
metabolism

53
Q

What are the possible causes of metastatic calcification?

A

Increased secretion of PTH‐ primary tumour of parathyroid, secondary to renal failure, ectopic

Destruction of bone tissue‐ primary tumour of bone marrow, Paget’s disease, immboilisation

54
Q

What is celluar aging?

A

Accumulation of damage to cellular constituents and DNA such as misfolded proteins

55
Q

What is replicative senescence?

A

Decline in a cell’s ability to replicate due to shortening of telomeres with every cell division

56
Q

How can cells overcome replicative senescence?

A

Some cells such as tumour cells produce telomerase which enables regeneration of the telomeres at the ends of chromosomes making the cell immortal

57
Q

What are the three main issues that occur as a result of chronic excess alcohol intake?

A

Fat change‐ steatosis leading to hepatomegaly, acute and reversible

Acute alcoholic hepatitis‐ due toxic alcohol and its metabolites, leads to mallory’s hyaline,
neutrophilic infiltrate and focal hepatitis necrosis, reversible

Cirrhosis‐ hard and shrunken liver, appears as micro‐nodules of regenerating hepatocytes surrounded by collagen bands, irreversible

Semester 2 - Mechanism of Disease (10 decks)

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