Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

8. MoD > 1. Cell Injury > Flashcards

1. Cell Injury Flashcards

1
Q

What is pathology the study of?

A

What went wrong.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is disease a consequence of?

A

Failed homeostasis with consequent morphological and functional disturbances.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What does the degree of cell injury depend on?

A

Type of injury, severity of injury, and type of tissue.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are some common causes of cell injury and death?

A

Hypoxia, toxins, physical agents, radiation, micro-organisms, immune mechanisms, dietary insufficiency and deficiencies or excess.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the four main causes of hypoxia?

A

Hypoxaemia hypoxia - arterial content of oxygen is low, from altitude.
Anaemic hypoxia - decreased ability of haemoglobin to carry oxygen.
Ischaemic hypoxia - interruption to blood supply, from heart failure.
Histiocytic hypoxia - inability to utilise oxygen in cells due to disabled oxidative phosphorylation enzymes, from cyanide poisoning.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How do neurones and fibroblasts differ in terms of how long they can tolerate hypoxia for before cell death or permanent damage?

A

Neurones - a few minutes.

Fibroblasts - a few hours.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Name two examples of toxin that can cause cell injury and death.

A

High concentration of oxygen, glucose and salt in hypertonic solutions, poisons, pollutants, insecticides, etc.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How can the immune system damage cells?

A

Hypersensitivity reactions where the host tissue is injured secondary to an overly vigorous immune reaction like with hives - inflammation in the skin.
Autoimmune reactions where the immune system fails to distinguish self from non-self, e.g. Graves disease.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the four principal targets for cell damage?

A

Cell membranes, nucleus, proteins, and mitochondria.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What happens in the cell in hypoxia?

A

Mitochondria reduce oxidative phosphorlyation so less ATP is made. This means the Na+ pump has less action so there is an influx of Ca2+, H2O and Na+ and an efflux of K+ which leads to cellular swelling etc. The lack of ATP means there has to be more glycolysis so pH decreases, as do glycogen stores. Low ATP means ribosomes detach from the endoplasmic reticulum so there is less protein synthesis and lipid deposition.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are free radicals?

A

Reactive oxygen species with a single unpaired electron in an outer orbit. It is unstable and highly reactive to produce more free radicals.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the three most biologically significant free radicals?

A

OH* - hydroxyl.
O2- - superoxide.
H2O2 - hydrogen peroxide.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How can free radicals be generated from H2O?

A

Radiation: H2O -> OH* + H*.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the Fenton reaction?

A

Fe2+ + H2O2 -> Fe3+ + OH- + OH*.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the Haber-Weiss reaction?

A

O2- + H+ + H2O2 -> O2 + H2O + OH*.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Why are lipids in the cell membranes a good target for free radicals?

A

It causes lipid peroxidation, this leads to further generation of further free radicals.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How do free radicals cause injury of proteins, carbohydrates, and DNA?

A

Causes the molecules to bend out of shape, so they become cross-linked. They’re then mutagenic.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

How does the body respond to free radicals?

A

Uses anti-oxidant system to remove them. Using: enzymes, free radical scavengers, or storage proteins.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

How does reperfusion after ischaemia cause injury?

A

If blood returns to damaged but not yet necrotic tissue, the damage is worse than if the blood flow hadn’t returned. From increased production of oxygen free radicals with reoxygenation, more neutrophils so more inflammation and injury, and delivery of complement proteins and activation of the complement pathway.

20
Q

What is the role of heat shock proteins?

A

Protection against cell injury. They mend or destroy mis-folded proteins to maintain cell viability.

21
Q

What is oncosis?

A

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

22
Q

How does oncosis present in light microscopy?

A

The cells have failed membrane and permeability so the cells shrink and the nucleus fragments.

23
Q

How does reversible cell injury present in electron microscopy?

A

Generalised swelling, clumping of chromatin, autophagy of lysosomes, ER and mitochondrial swelling, blebs.

24
Q

How does irreversible cell injury present in electron microscopy?

A

Rupture of lysosomes and autolysis, defects in cell membranes, myelin figures, lysis of ER, nucleus pyknosis, karyolysis or karyorrhexis.

25
Q

What is necrosis?

A

The morphological changes in a living organism that occur after a cell has been dead some time.

26
Q

What is apoptosis?

A

Cell death with shrinkage, programmed by the cell.

27
Q

What are the major differences between apoptosis and oncosis?

A

Apoptosis is ATP dependent, oncosis is ATP independent. Apoptosis has cell shrinkage, but oncosis has cell swelling.

28
Q

What are the two main types of necrosis?

A

Liquefactive and coagulative.

29
Q

What are the two prominent types of necrosis in clinical practice?

A

Caseous and fat necrosis.

30
Q

How are protein denaturation and enzyme release linked to liquefactive and coagulative necrosis?

A

Liquefactive necrosis has more enzyme release, coagulative has more protein denaturation.

31
Q

How does caseous necrosis present?

A

Contains amorphous/ structureless debris. Associated with infections like tuberculosis.

32
Q

What is fat necrosis from?

A

The destruction of adipose tissue, releases fatty acids that react with calcium to form chalky deposits in the tissue.

33
Q

What are the two types of gangrene?

A

Dry and wet (one subtype is gas gangrene).

34
Q

What is the difference between white and red infarct?

A

White infarct has no blood in it, occurs at end artery sites, coagulative necrosis.
Red infarct is haemorrhagic so has lots of blood in it, in organs with dual blood supply.

35
Q

What do the consequence of infarcts depend on?

A

Alternative blood supply, speed of ischaemia, tissue involved and oxygen content of the blood.

36
Q

What is a physiological use of apoptosis?

A

Sculpting in embryology.

37
Q

When is apoptosis pathological?

A

When the cell is damaged and needs to be removed.

38
Q

What are the stages of structural change in apoptosis?

A

Normal cell -> condensation -> fragmentation -> apoptic bodies.

39
Q

What are the three phases of apoptosis?

A

Initiation, execution and degradation and phagocytosis.

40
Q

What happens in intrinsic initiation and execution of apoptosis?

A

DNA damages means p53 is activated. The mitochondria is a key player in this, it releases apoptosomes that activate caspase-9 and promote apoptosis.

41
Q

What happens in extrinsic initiation and execution of apoptosis?

A

It’s outside the cell and leads to activated caspase-8 leading to apoptosis.

42
Q

What are the changes in a cell over degradation and phagocytosis in apoptosis?

A

Loss of microvilli and junction and nuclear changes. Then apoptic body and fragmentation. Phagocytosis and apoptic bodies are separated.

43
Q

What are some key apoptic molecules?

A

p53 - in response to DNA damage.
Cytochrome c, APAF1, caspase 9 - apoptosome.
Bcl-2 - inhibits apoptosis by preventing mitochondrial release of cytochrome c.
Death ligands.
Death receptors.
Caspases - effector molecules of apoptosis.

44
Q

What can abnormal accumulations be a result of?

A

Cell’s own metabolism, extracellular space, the outer environment.

45
Q

What are the five main groups of intracellular accumulations?

A

Water and electrolytes, lipids, carbohydrates, proteins and pigments.

46
Q

What is dystrophic calcification?

A

Local calcification.

47
Q

What is a cause of pathological metastatic calcification?

A

Destruction of bone in bone cancers or parathyroid tumours.

8. MoD (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions