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SOPHIE'S ESA 2 > MoD Session 1- Cell Injury > Flashcards

MoD Session 1- Cell Injury Flashcards

0
Q

What 4 factors does the degree of cell injury depend on?

A
  • type of tissue
  • type of injury
  • duration of injury
  • severity of injury
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1
Q

What is disease a failure of?

A

Homeostasis

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2
Q

What is hypoxia and how does it cause cell injury?

A

It is oxygen deprivation.

It can cause decreased aerobic respiration and therefore cell injury.

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3
Q

What is Ischaemia and why is it more dangerous than hypoxia?

A

It is a reduction blood supply, therefore causing a reduced supply of oxygen and metabolic substrates.

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4
Q

What are the four causes of hypoxia?

A
  • hypoxaemic hypoxia- less arterial oxygen
  • histiocytic hypoxia- disabled oxidative phosphorylation enzymes
  • anaemia hypoxia- inability of haemoglobin to carry oxygen
  • ischaemic hypoxia- reduced blood supply.
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5
Q

What are some of the physical agents that cause cell injury? (5 max)

A 
Temperature extremes 
Radiation 
Direct trauma 
Electric currents 
Atmospheric pressure changes
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6
Q

What are toxins that cause cell injury? (4 max)

A
  • insecticides, herbicides
  • pollutants, poisons, asbestos
  • alcohol and drugs
  • high oxygen conc.
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7
Q

What are micro-organisms that cause cell injury? (3)

A
  • fungi
  • bacteria
  • viruses
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8
Q

What two immune mechanisms can cause cell injury?

A
  • hypersensitivity reactions

- autoimmune reactions

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9
Q

What are the 7 causes of cell injury?

A
  • hypoxia
  • immune mechanisms
  • dietary imbalance
  • genetic abnormalities
  • toxins
  • micro-organisms
  • physical agents
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10
Q

What are 4 target sites for cell injury?

A
  • nucleus
  • mitochondria
  • cell membranes
  • proteins
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11
Q

What are the three main consequences of reversible hypoxia injury?

A
  • ribosomes detach from the ER as there is less ATP therefore less protein synthesis and increased lipid deposition.
  • NA+/K+ pump activity is reduced therefore high intracellular sodium and water follows= swelling.
  • more glycolysis- more lactic acid production. Low pH affects enzyme activity.
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12
Q

Why does irreversible injury eventually occur as a result of hypoxia?

A

Membrane integrity is disturbed and it becomes increasingly permeable.
Entry of calcium activates enzymes which destroy the cell.

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13
Q

What is ischaemic reperfusion injury?

A

When a tissue injury is worsened by the return of blood flow to a damaged, but not yet necrotic tissue.

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14
Q

What are free radicals and give the three most important examples.

A

They are reactive oxygen species with a single unpaired electron in their outer orbit that can react with other molecules to produce more free radicals.
H2O2, OH. , O2-

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15
Q

What are the body’s defence against free radicals? (2)

A
  • heat shock proteins - increased production when the body is in oxidative stress. They repair misfolded proteins to maintain cellular viability.
  • anti-oxidants- SOD, catalase and peroxidases remove free radicals, scavengers such as Vit A,C and E, and glutathione neutralise them.
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16
Q

What are the reversible and irreversible cytoplasmic changes under the L microscope?

A
  • reversible- reduced pink staining due to increased water accumulation
  • irreversible- dark oink staining due to detached ribosomes and protein denaturation.
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17
Q

What acre the reversible and irreversible nuclear changes seem under the L microscope?

A
  • reversible- chromatin clumping

- irreversible- pyknosis, karryolysis, karryohexis

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18
Q

What are some of the reversible features seen under the electron microscope?

A
  • blebbing
  • swelling- sodium potassium pump failure
  • chromatin clumping
  • ribosome separation
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19
Q

What are some of the irreversible features seen under the electron microscope?

A
  • myelin figures
  • membrane defects
  • ER lysis
  • cell swelling
  • pyknosis, karryohexis, karryolysis
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20
Q

Define oncosis

A

Cell death with swelling.

It is a change that occurs in cells prior to death.

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21
Q

Define apoptosis

A

Cell death with shrinkage.

Cell suicide

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22
Q

Define necrosis

A

It is not a process, but an appearance of cell death. Morphological changes that occur 4-24 hours after cell death.
Also sees swelling.

23
Q

Which the of necrosis appears white, is denatured proteins and therefore is firm and has a ghost outline?

A

Coagulative

24
Q

Which type of necrosis occurs due to neutrophil death and is digestion of tissues?

A

Liquefactive

25
Q

Where is Liquefactive necrosis typically found?

A

The brain

26
Q

What type of necrosis has amorphous debris and a cottage cheese like appearance?

A

Caseous

27
Q

What is caseous necrosis associated with?

A

Infection. E.g TB

28
Q

When does fat necrosis occur? (2)

A
  • as a result of direct trauma to adipose

- following acute pancreatitis as lipases are released which act on adipose.

29
Q

What is a characteristic feature of fat necrosis?

A

Chalky deposits due to the release of fatty acids reacting with calcium.

30
Q

What is gangrene?

A

A description of necrosis.

31
Q

What is dry gangrene?

A

Coagulative necrosis modified by exposure to the air.

32
Q

What is wet gangrene?

A

Liquefactive necrosis infected with a mixed bacterial culture.

33
Q

Why is wet gangrene serious?

A

Because bacteria can easily get into the blood stream and cause septicaemia.

34
Q

What is gas gangrene and when is it most common?

A

It is wet gangrene caused by anaerobic bacteria that produce visible, palpable gas bubbles.
Ischaemic limbs.

35
Q

What is an infarct?

A

An ischaemic necrosis

36
Q

When do white infarcts occur, and why are they white?

A

They occur in solid organs due to the occlusion of an end artery.
They are white because there is a lack of blood.

37
Q

When do red infarcts occur?

A

They occur when there is extensive haemorrhage into dead tissue.

38
Q

Why are molecules released during cell injury?

A

Because membrane integrity is lost.

39
Q

What are the 3 molecules released by injured cells?

A
  • potassium
  • enzymes
  • myoglobin
40
Q

When are budding and blebbing seen?

A
  • budding- apoptosis

- blebbing- oncosis

41
Q

What are the three steps of apoptosis and what happens at each?

A
  1. Initiation - intrinsic and extrinsic mechanisms activate caspases that cleave proteins and initiate DNA degradation.
  2. Execution - intrinsic- mitochondria becomes more permeable and cytochrome C is therefore released. Extrinsic- Ligands bind to death receptors.
  3. Degradation and phagocytosis - cell breaks down into apoptotic bodies which induce phagocytosis.
42
Q

What are two important apoptotic molecules?

A

P53- mediates apoptosis in response to DNA damage

BC1-2- prevents cytochrome C release from mitochondria, therefore inhibits apoptosis.

43
Q

Why can fluid accumulate in cellular damage?

A

Due to osmotic disturbances.

44
Q

What lipids can accumulate abnormally? And where do they accumulate?

A
  • triglycerides. - cause steatosis. Common in the liver as this is the site of metabolism.
  • cholesterol. - excess is stored in membrane bound droplets and can cause xanthomas and atheromas.
45
Q

What proteins can accumulate in cellular damage?

How do they accumulate?

A
  • Mallorys hyaline- they accumulate due to damaged protein in hepatocytes as a result of alcoholic liver disease. It is an accumulation of altered keratin filaments.
  • alpha-1-anti trypsin- deficiency of this is a genetic disorder in which the liver incorrectly folds it and therefore it can’t be packaged by the ER, so accumulates and isn’t secreted by the liver.
46
Q

What exogenous pigments can accumulate in cells?

A
  • tattoos- pigment placed into skin is phagocytosed by macrophages.
  • carbon, coal dust and soot- are inhaled and then phagocytosed as above to give blackened lungs.
47
Q

What endogenous pigments can accumulate? (3)

A
  • lipofuscin
  • haemosiderin
  • bilirubin
48
Q

What is haemosiderosis?

A

When there is deposition of haemosiderin due to a systemic iron overload.

49
Q

What is hereditary haemochromatosis?

A

A genetically inherited disorder leading to increased intestinal iron absorption causing haemosiderosis in various organs.

50
Q

Where do dystrophic and metastatic calcifications occur, respectively?

A
  • dystrophic- dying tissues e.g atherosclerotic plaques and damaged heart valves.
  • metastatic- body wide distribution.
51
Q

What is pathological calcification?

A

Abnormal deposition of calcium salts (hydroxyapatite crystals) within tissues.

52
Q

What is metastatic calcification due to?

A

Hypercalcaemia caused by disturbance in calcium metabolism.

53
Q

What is replication senescence?

A

When cells can no longer replicate because they have reached their critical length.

54
Q

What are the results of chronic alcohol intake and why do they arise? (3)

A
  • fatty change- fat metabolism is affected, therefore steatosis occurs and hepatomegaly as a result.
  • acute alcoholic hepatitis- alcohol and metabolites are toxic, therefore in high quantities they can cause hepatitis, necrosis, Mallory bodies and neutrophil infiltration.
  • cirrhosis- a hard, shrunken, nobbly liver.
55
Q

Which two consequences of excessive alcohol intake are often reversible and which one is irreversible?

A
  • reversible- fatty change and hepatitis

- irreversible- cirrhosis

SOPHIE'S ESA 2 (74 decks)

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