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Mechanisms of Disease > Cell Injury > Flashcards

Cell Injury Flashcards

0
Q

What are the causes of hypoxia?

A

Hypoxaemic (arterial content of oxygen is low), anaemic (inability to transport oxygen), ischaemic (interruption of blood supply) and histiocytic (inability to utilise oxygen in cells e.g. cyanide poisoning)

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1
Q

What are the common causes of cell injury?

A

Hypoxia, physical agents, chemical agents & drugs, microorganisms, immune mechanisms, diet and genetic abnormalities

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2
Q

What are the four essential cell components that are the principle targets of cell injury?

A

Cell membranes, nuclei, proteins and mitochondria

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3
Q

How does reversible hypoxic injury occur?

A

Decreased levels of ATP –> loss of activity of Na+/K+ pumps –> increase in cellular Na+ –> oncosis –> gycolytic pathway is activated –>build up of lactic acid –> chromatin clumping –> detachment of ribosomes

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4
Q

How does irreversible hypoxic injury occur?

What does it usually appear as?

A

Ca2+ increases intracellularly –> activation of enzymes (e.g. ATPases, proteases etc) –> leakage of these enzymes.
Usually appears as necrosis.

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5
Q

How does ischaemic-reperfusion injury occur?

A

When blood flow is returned to a tissue which has been subjected to ischaemia, but is not yet necrotic

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6
Q

Give three possible causes of ischaemic-reperfusion injury

A

Increased production of free radicals
Increased number of neutrophils resulting in inflammation
Delivery of complement proteins and activation of the complement pathway

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7
Q

How does chemical injury occur?

A

Chemicals can act by combining with a cellular component e.g. cyanide binding to mitochondrial cytochrome oxidase and blocks oxidative phosphorylation

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8
Q

How do free radicals cause cell damage?

A

They react with other molecules and attack lipids in cell membranes and cause lipid peroxidation. They can also damage proteins and nucleic acids

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9
Q

What are the three main free radicals?

A

Hydroxyl (OH-), superoxide (O2-) and hydrogen peroxide (H2O2)

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10
Q

How can hydroxyl radicals be produced?

A

Radiation which directly lyses water
Fenton and Haber-Weiss reactions

F: Fe2+ + H2O2 –> Fe3+ + OH- + OH (free radical)
H&W: O2- + H+ + H2O2 –> O2 + H2O + OH (free radical)

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11
Q

What does the body’s anti-oxidant system consist of?

A

Enzymes (e.g. SOD, catalases and peroxidases)
Free radical scavengers (vits ACE and glutathione)
Storage proteins (e.g. transferrin and cerruloplasmin)

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12
Q

What is the function of heat shock proteins?

A

They ensure that proteins are re folded properly, if this is not possible the protein is destroyed. Maintain a role in protein viability, thus maximising cell survival - e.g. unfoldases or chaperonins

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13
Q

What three main alterations can be seen with a light microscope?

A

Cytoplasmic changes e.g. reduced staining of cytoplasm due to accumulation of water (can be followed by increased staining)
Nuclear changes e.g. chromatin clumping, pyknosis, karryohexis and karryolysis
Abnormal intracellular accumulations

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14
Q

Define apoptosis

A

Cell death regulated by intracellular programming whereby a cell activates enzymes that degrade its own nuclear DNA and proteins

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15
Q

Give some examples of apoptosis

A

Hormone controlled involution
Cytotoxic T cells killing virus infected cells
Embryogenesis

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16
Q

Is apoptosis active or passive?

A

Active

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17
Q

How to apoptotic cells appear under a light microscope?

A

Shrunken and intensely eosinophilic. Chromatin condensation, pyknosis and nuclear fragmentation

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18
Q

How do apoptotic cells appear under electron microscopes?

A

Cytoplasmic blebbing which progresses to fragmentation into apoptotic bodies.

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19
Q

What are the three key phases of apoptosis?

A

Initiation, execution and degradation/phagocytosis

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20
Q

What is pyknosis?

A

Shrinkage

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21
Q

What is karryohexis?

A

Fragmentation

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22
Q

What is karryolysis?

A

Dissolution

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23
Q

How are reversible changes seen under an electron microscope?

A

Swelling, cytoplasmic blebs, chromatin clumping, ribosome separation from ER

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24
Q

How do irreversible cell changes appear under electron microscopes?

A

Further swelling, nuclear changes, ruptured lysosomes, membrane defects, myelin figures, lysis of ER, amorphous densities in swollen mitochondria

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25
Q

Define oncosis

A

Spectrum of changes that occur in injured cells prior to death

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26
Q

Define necrosis

A

Morphological changes following cell death in living tissue, largely due to progressive degradative changes due to action of enzymes

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27
Q

What is dystrophic calcification?

Where does it occur?

A

Calcification of necrotic tissue damage.

Occurs in areas of dying tissue, ageing or damaged heart vessels and in tuberculus lymph nodes

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28
Q

What are the two main types of necrosis?

What are the other two types?

A

Coagulative and liquifactive

Caseous and fat

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29
Q

Define embolus

A

A particle that travels in the blood supply and gets lodged at a site that is separate from the site of production

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30
Q

What happens in intrinsic initiation of apoptosis?

Where does it occur?

A

Triggers lead to increased permeability, resulting in release of cytochrome c from mitochondria. Interacts with APAF1 and capsase 9 to form an apoptosome that activates various downstream capsases

Occurs in the mitochondria

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31
Q

What happens in extrinsic initiation of apoptosis?

What is this process mediated by?

A

External ligands (e.g. TRAIL and Fas) bind to ‘death receptors’ leading to capsase activation independently of mitochondria

It is receptor mediated

32
Q

What occurs in the degradation/phagocytosis step of apoptosis?

A

Cell breaks into membrane bound fragments (apoptotic bodies)

33
Q

List some important apoptotic molecules

A

p53 (mediates apoptosis in response of DNA damage)
Cytochrome c, APAF1, capsase 9 (form apoptosome)
Bcl-2 (inhibits apoptosis)
Death ligands/receptors (e.g. TRAIL and TRAIL-R)
Capsases (effector molecules of apoptosis)

34
Q

Give some examples of substances that can accumulate intracellularly

A

Normal cell constituents e.g. water, lipids, proteins etc
Abnormal substances e.g. minerals
Pigments

35
Q

What is steatosis?

A

Accumulation of triglycerides

36
Q

What are the common causes of liver steatosis?

A

Alcohol abuse, diabetes mellitus, obesity and toxins (e.g. carbon tetracholride)

37
Q

What is steatohepatitis?

Is it reversible or irreversible?

What can occur if steatohepatitis progresses?

A

Fatty liver disease.
When there is just an accumulation of fat it is reversible. Once inflammation occurs this process is irreversible because the inflammation is replaced by connective tissue, resulting in cirrhosis.

38
Q

What is Mallroy’s hyaline?

How does it occur?

A

Damaged protein seen in hepatocytes in alcoholic liver disease.
It occurs as a result of accumulation of altered keratin filaments

39
Q

What is alpha 1-antitrypsin deficiency?

What can patients develop?

A

It’s a genetically inherited disorder in which the liver produces a version of the protein alpha 1-antitrypsin that’s incorrectly folded. This cannot be packaged by ER and accumulates.
Patients can develop emphysema as lung tissue gets broken down

40
Q

What is anthracosis?

What can it lead to if exposure is over a long period of time?

A

Blackened lung tissue or as blackened peribronchial lymph nodes
Lungs can become fibrotic or emphysematous (coal workers pneumoconiosis)

41
Q

What is lipofusin and where is it seen?

What is it indicative of?

A

Lipofusin is a brown pigment seen in aging cells. It doesn’t cause injury to the cell although it is a sign of previous free radical injury and lipid peroxidation

42
Q

What is haemosiderin? Where is it derived from?

A

Haemosiderin is a yellow/brown pigment and it contains iron.
Derived from Hb and is formed when there is a systemic or local excess of iron

43
Q

What can lead to haemosiderin deposition?

A

Haemolytic anaemias, blood transfusions and hereditary haemochromatosis

44
Q

What is pathological calcification?

A

Abnormal deposition of calcium salts within tissues. Can be dystrophic or metastatic

45
Q

What is metastatic calcification?

A

Calcium deposition when there is hypercalcaemia secondary to disturbances in calcium metabolism. It’s usually asymptomatic.

46
Q

What are the four main causes for metastatic calcification?

A

Renal failure
Vitamin D related disorders
Destruction of bone secondary to primary tumours of bone e.g. leukaemia, metastases to bone, Paget’s disease or immobilisation
Increased secretion of PTH

47
Q

What is replicative senescence?

A

Decline in cells’ ability to replicate

48
Q

What stops cells replicating non-stop?

A

Telomeres are shortened each time the cell replicates and they will eventually reach a critical length

49
Q

What mechanisms do germ cells have to prevent shortening of telomeres?

A

They contain an enzyme called telomerase which maintains the original length of the telomeres

50
Q

How can metabolic tolerance of alcohol occur?

A

Induction of CYP2E1, which increases the rate of metabolism of ethanol

51
Q

What is ethanol metabolised to?

Which enzymes are involved?

A

Acetaldehyde

CYP2E1, catalase and alcohol dehydrogenase

52
Q

What is fatty change?

Is it reversible or irreversible?

A

Toxicity of alcohol to the liver resulting in steatosis which can cause hepatomegaly
It’s reversible and generally asymptomatic

53
Q

What is acute alcoholic hepatitis?

Is this reversible or irreversible?

A

Occurs after binge drinking. There will be focal hepatocyte necrosis, formation of Mallory’s bodies and neutrophilic infiltrate.
Usually reversible

54
Q

What is cirrhosis?

Is it reversible or irreversible?

A

Hard, shrunken liver. Histologically - micronodules of regenerating hepatocytes surrounded by bands of collagen.

Irreversible and sometimes fatal

55
Q

Where is paracetamol detoxified?

How is this done?

A

Liver.
Occurs by sulphonation and glucuronidation. Small amounts are metabolised by CYP2E1 to NAPQI which is then detoxified by interaction with glutathione.

56
Q

When is liver necrosis seen?

A

In paracetamol overdoes, around about 3-5 days after the overdose
(NB: liver necrosis is not seen in alcohol overdose)

57
Q

What can be given to a person who has taken a paracetamol overdose?
How do you determine whether or not to give this to them

A

NAC. 4 hours after the overdose the serum concentration of paracetamol is measured.

58
Q

How can you check for the severity of liver damage in patients with paracetamol overdose?

A

INR time is measured 24 hours after the overdose for a guide.

59
Q

What does an aspirin overdose result in?

A

Respiratory alkalosis. Compensatory mechanisms result in metabolic acidosis.

60
Q

What happens after an aspirin overdose?

A

Acetylation of platelet cyclooxygenase and blockage of platelets ability to make thromboxane A2

61
Q

What does inhibition of platelet cyclooxygenase cause?

A

Decreased platelet aggregation and petechaie. Can also result in acute erosive gastritis producing GI bleeding.

62
Q

What type of necrosis is protein degeneration more predominant in?
What is the converse of this?

A

Coagulation necrosis

Conversely when release of enzymes is more dominant the type of necrosis is liquefactive

63
Q

Describe what you would see in coagulative necrosis.

A

Ghost outline of cells (in the first few days). After this the appearance is modified by acute inflammation incited by dead tissue leading to consequent infiltration by phagocytes

64
Q

Where would you see liquefactive necrosis?

A

Massive neutrophil infiltration (abscess). Bacterial infections. Also seen in the brain because its a fragile tissue without support from a robust collagenous matrix

65
Q

How does caseous necrosis appear macroscopically?

A

Has a cheesy appearance

66
Q

What is caseous necrosis associated with?

A

Infections - TB. Often associated with a particular form of inflammation known as granulomatos

67
Q

When is fat necrosis seen?

A

Most typically seen as a consequence of of acute pancreatitis. Can also occur after direct trauma to fatty tissue (especially breast tissue) - can leave an irregular scar that can mimic a nodule of breast cancer

68
Q

What is gangrene?
What are the types?
What is the clinical relevance?

A

Necrosis that is visible to the naked eye.
Can be wet or dry, wet gangrene is typically due to infection and can result in septicaemia (needs urgent attention).
NB: gangrene is not a type of necrosis, it’s a clinical term used to describe necrosis

69
Q

What are possible causes for infarction?

A

Emboli, thrombi, external compression of a vessel (e.g. by a tumour) or twisting of vessels (e.g. testicular torsion)

70
Q

How do white infarcts occur?

How do they appear histologically?

A

Occur due to an occlusion of an end artery. Solid nature of tissue limits the amount of haemorrhage that can occur.
They appear as coagulative necroses

71
Q

Where does white infarction occur?

A

They occur in solid organs (good stromal support) e.g. kidney, heart and spleen

72
Q

When do red infarcts occur?

A

When there is excessive haemorrhage into dead tissue. In organs with dual blood supply, numerous anastomoses or in loose tissue.

73
Q

What would you see in lab tests in a patient with hepatitis?

What further tests could you do?

A

HPV would be elevated. ALT and AST might be elevated due to liver damage.
Serologic tests to detect HCV antibodies, molecular tests to detect and quantitate HCV RNA, and genotyping techniques.

74
Q

What would you see in lab tests for a patient with alcoholic liver disease?

A

GGT, ALT & AST can be elevated in alcoholic liver disease. If AST more than twice the ALT - liver disease likely

75
Q

What would you see in the lab tests of a patient with acute pancreatitis?

A

Pancreatic amylase and lipase are typically elevated to three times their usual amount

76
Q

What are you likely to see the lab test results of a patient who had an MI?

A

Troponin T and I are likely to be elevated. These need to be measured at presentation and ten 10-12 hours after presentation as well. Enzyme - creatine kinase is likely to be elevated

77
Q

What are the 6 p’s of ischaemia?

A

Pallor, perishingly cold, parasthesia, pulselessness, pain, paralysis

78
Q

What is Laplace’s law?

A

For a given internal fluid pressure for a vessel, the wall tension is proportional for a radius of vessel. Therefore in an aneurysm - increased radius therefore you need a thicker wall to cope with it.

Mechanisms of Disease (8 decks)

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