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Pathological Processes > Session 1 > Flashcards

Session 1 Flashcards

1
Q

What is hypoxaemic hypoxia?

What can cause this?

A

Low arterial oxygen content.

Altitude or lung disease

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2
Q

What is anaemic hypoxia?

What can cause this?

A

Decreases ability of Hb to carry oxygen.

Anaemia or CO poisoning

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3
Q

What is ischaemic hypoxia?

What can cause this?

A

Interruption to blood supply.

Blockage of a heart vessel or heart failure.

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4
Q

What is histiocytic hypoxia?

What can cause this?

A

Inability to utilise oxygen in cells due to disabled oxidative phosphorylation.
Cyanide poisoning

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5
Q

What two ways can the immune system cause cell damage?

A

Hypersensitivity reactions eg urticaria (hives). The body creates an overly vigorous immune response.
Autoimmune reactions eg Graves disease. The body cannot recognise self from non self.

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6
Q

Which 4 cell components are most susceptible to injury?

A
  1. Cell membranes
  2. Nucleus (DNA)
  3. Proteins (structural or enzymes)
  4. Mitochondria (ox phos)
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7
Q

Describe what happens to the ion channels in reversible hypoxia.

How does this lead to swelling?

A
  1. Mitochondria can no longer carry out oxidative phosphorylation.
  2. This leads to less ATP so Na+/K+ ATPase can no longer pump Na+ out of cell.
  3. Na+ accumulates in cell which causes NCX to reverse.
  4. Influx of Ca+, Na+ and H2O
  5. Efflux of K+
  6. Causes cellular swelling, loss of microvilli, blebs, ER swelling, myelin figures.
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8
Q

What are the 2 side effects of reversible hypoxia apart from swelling?

A
  1. More glycolysis which lowers cellular pH and glycogen stores. Clumping of nuclear chromatin.
  2. Ribosomes detach so protein synthesis lowers. Leads to lipid deposition.
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9
Q

What is irreversible hypoxic injury?

What 4 enzymes are involved and what do they do?

A

When cytosolic calcium becomes too high. Activates destructive enzymes.

  1. ATPase - decreases ATP
  2. Phospholipase - Decreases phospholipids
  3. Protease - Disrupts membrane and cytoskeletal proteins
  4. Endonuclease - Nuclear chromatin damage
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10
Q

What are the 3 most important free radicals?

A

Hydroxyl (most dangerous)
Superoxide
Hydrogen peroxide

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11
Q

What are the sources of oxidative damage? (6)

A
  1. Ox Phos
  2. Inflammation (oxidative burst of neutrophils)
  3. Radiation
  4. Contact with unbound iron (Fenton reaction)
  5. Contact with unbound copper (Wilsons disease)
  6. Drugs eg paracetamol
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12
Q

What are heat shock proteins?
What are the two types?
Give a names example

A

Heat shock response aims to mend misfolded proteins and maintain cell viability.
Unfoldases or chaperonins in the RER
eg ubiquitin

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13
Q

What changes can you see under a light microscope from hypoxic cells?

A
  1. Cytoplasmic changes
  2. Nuclear changes
  3. Abnormal intracellular accumulations
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14
Q

What changes can you see from an electron microscope of reversible hypoxia?

A
  1. Blebs (protrusions of outer membrane
  2. Generalised, ER, mitochondrial swelling
  3. Autophagy by lysosomes
  4. Clumping of nuclear chromatic
  5. Dispersion of ribosomes
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15
Q

What changes can you see from an electron microscope of irreversible hypoxia?

A
  1. Rupture of lysosomes and autolysis
  2. Nucleus pyknosis/karyolysis/karyorrhexis
    Pyknosis - Condensation of chromatin (reversible)
    Karyorrhexis- Fragmentation of the nucleus
    Karyolysis - Nucleus dissolution
    3.Defects in cell membrane
  3. Lysis of ER
  4. Myelin figures
  5. Large densities in mitochondria
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16
Q

Define oncosis

A

Cell death with swelling, the spectrum of changes that occur in injured cells prior to death.

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17
Q

Define necrosis

A

In a living organism, the morphologic changes that occur after a cell has been dead some time. Seen after 12-24 hours.

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18
Q

What is coagulative necrosis?

Where does this occur?

A

Due to protein denaturation. Cellular architecture is preserved, giving a ghost outline of cells.
eg solid organs like the heart

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19
Q

What is liquefactive necrosis?

Where does this occur?

A

Due to enzyme degradation, leading to enzymatic digestion of the tissues. There is a presence of mamy neutrophils.
eg brain, loose tissues

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20
Q

What is caseous necrosis?
What does this look like?
Where does this occur?

A

Contains amorphous debris, associated with infections eg TB
Looks like cheese, some ghost outlines
Happens in the tubercles

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21
Q

What is fat necrosis?

Where can this happen?

A

Fat cells are broken down by the body in response to trauma. Fatty acids react with calcium which creates chalky deposits.
Happens in breast tissue and pancreas

22
Q

Define gangrene

A

Necrosis visible to the naked eye

23
Q

Define infarction

What can this result in?

A

Necrosis to an area caused by the reduction in arterial blood flow, can result in gangrene

24
Q

Define infarct

A

An area of necrotic tissue which is the result of loss of arterial blood supply ie an area of ischaemic necrosis

25
Q

Define dry gangrene

A

Necrosis modified by exposure to air (coagulative necrosis)

26
Q

Define wet gangrene

A

Necrosis modified by infection

27
Q

Define gas gangrene

A

Wet gangrene where the infection is with anaerobic bacteria that produce gas

28
Q

What are the commonest causes of infarction

A

Thombosis (blood clot in a coronary artery)

Ebolism (blood clot distant from point of origin)

29
Q

Why are some infarcts white?

Where do they happen?

A

Happens in solid organs, due to obstruction of an end artery. Example of coagulative necrosis. Often wedge shape.

30
Q

Why are some infarcts red?

When do they happen?

A

Occurs in loose tissues with a dual blood supply or numerous anastomoses. Due to bleeding into the infarct.
eg lungs or intestine

31
Q

What is ischaemia-reperfusion injury?

what are the 3 causes?

A

If tissue is subject to ischaemia but not yet necrotic, the tissue injury sustained can be worse.
This can be due to:
1. Increased of ROS due to a burst in mitochondrial activity
2. Increased neutrophils causing inflammation and acute tissue injury.
3. Delivery of compliment proteins and activation of complement pathway.

32
Q

What 3 molecules are released in injured celled?

A
  1. Potassium = toxic
  2. Enzymes
  3. Myoglobin
33
Q

Define apoptosis

A

Cell death with shrinkage, induced by a regulated intracellular program where a cell activates enzymes to degrade it’s own nuclear DNA and proteins. Non random cleavage of DNA, no lysosomal enzymes, maintenance of membrane integrity.

34
Q

When does apoptosis occur? 3

A
  1. In order to maintain a steady state
  2. Hormone controlled involution
  3. Embryogenesis
35
Q

When does apoptosis occur pathologically? 3

A

Cytotoxic T cell killing of virus infected or neoplastic cells.
When cells have DNA damage
Graft vs host disease

36
Q

What are the 4 visual stages of apoptosis?

A
  1. Normal cell
  2. Condensation
  3. Fragmentation
  4. Apoptic bodies
37
Q

What is the intrinsic initiation pathway of apoptosis?

A
  1. DNA damage/withdrawal of growth factors/hormone
  2. p53 protein activated
  3. Outer mitochondrial membrane becomes leaky
  4. Cytochrome C is released from mitochondria and this activates caspases
38
Q

What is the extrinsic initiation pathway of apoptosis?

A
  1. Tumour cell/virus cell
  2. TNFa released by T killer cells
  3. Bind to cell membrane receptor (death receptor)
  4. Activates caspases
39
Q

What are caspases?

A

Enzymes that control and mediate apoptosis. Cause cleavage of the DNA and proteins of the cytoskeleton.

40
Q

How are apoptotic bodies removed?

A

They express proteins on their surface that are recognised by phagocytes/neighbour. They degrade the cell.

41
Q

Compare necrosis to oncosis

A

Oncosis - Contiguous groups of cells, swelling, nucleus (pynosis, karyorrhexis, karyolysis), lysis of cell membrane, contents digests and leak out of cell, adjacent inflammation, pathologic
Necrosis - Single cells, shrinkage, fragmentation of nucleus into fragments, plasma membrane intact, cellular contents intact into apoptotic bodies, no adjacent inflammation, mostly physiologic

42
Q

When does fluid accumulate in cells?
What is this called?
Where is it a bad problem?

A

Hydropic swelling.
Occurs during hypoxia - Na+ and H20 in
Particular problem in the brain

43
Q

Where do lipids accumulate in cells?
What is this called?
Causes?
What does it look like under microscopy?

A

Liver, xanthomas, smooth muscle as plaques.
Steatosis
Alcohol, diabetes mellitus, obesity, toxins (carbon tetrachloride)
-Looks like needles under microscopy.

44
Q

What does protein accumulation look like in cells?

What are the two causes?

A

Eosinophillic droplets or cytoplasmic aggregation

  1. Alcoholic Liver Disease - Damaged keratin filaments called Mallory’s Hyaline
  2. a1- antitrypsin deficiency, incorrectly folded so accumulated in ER. Causes emphysema in the lungs.
45
Q

What are 2 exogenous sources of pigments in cells?

How can this cause anthracosis and coal workers pneumoconiosis?

A

Tattoos
Coal dust is inhaled and phagocytosed by alveolar macrophages = anthracosis.
With fibrosis and emphysema = coal workers pneumoconiosis.

46
Q

What is haemosiderin?

What happens if there is too much iron in the body?

A

An endogenous source of pigment within cells. It is an iron storage molecule, derived from Hb. Forms where there is a local excess of iron eg bruising
Too much iron = It is deposited in organs, causing haemosiderosis

47
Q

What is hereditary haemochromatosis?

A

Genetically inherited disorder where too much iron is absorbed at the intestine. Deposited in the skin, liver, heart and endocrine organs etc
Causes cirrhosis and scarring of pancreas/
Symptoms - Liver damage, heart disfunction, endocrine failures. ‘bronze diabetes’, looking tan.
Treatment - Repeated bleeding.

48
Q

What is bilirubin?

How can jaundice occur?

A

An endogenous pigment of the skin. It is a breakdown product of Heme (porphyrin rings). Taken from tissues by albumin to liver and it is excreted in bile.
If too much = Jaundice
Deposited in tissues extracellularly or macrophages.

49
Q

What is dystrophic calcification?
What is the cause?
Where does it occur?

A

Localised deposition of calcium salts within tissues.
Occurs in areas of dying tissue, plaques, aging/damages heart valves, malignancies.
Cause: Local change favours nucleation of hydroxyapatite crystals. No abnormal metabolism.

50
Q

What is metastatic calcification?

A

Generalised deposition of calcium salts within tissues.
Cause = Increased secretion of PTH, resulting in bone resorption.
Primary - Tumour of parathyroid gland
Secondary - Renal failure/phosphate retention
Ectopic - Secretion of PTH related protein by tumours
Cause = Destruction of bone tissues
- Immobilisation, bone marrow tumours, Pagets disease.

51
Q

What is replicative senescence?

A

As cells age they accumulate DNA damage. After a certain number of divisions, the telomeres are too short so the cell can no longer divide.

52
Q

How do stem cells and cancer cells continue replication forever?

A

Contain an enzyme called telomerase which maintains length of the telomeres.

Pathological Processes (2 decks)

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