Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

ESA 2 - Pathological Processes > Session 1: Cell Injury > Flashcards

Session 1: Cell Injury Flashcards

(90 cards)

Start Studying
1
Q

What kind of things can cause cell injury?

A
  • hypoxia
  • toxins
  • physical agents (direct trauma, extremes of temperature, changes in pressure, electric currents)
  • radiation
  • microorganisms
  • immune mechanisms
  • dietary insufficiency and deficiencies, dietary excess
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the difference between hypoxia and ischaemia?

A

Hypoxia - decreased oxygen supply

Ischaemia - decreased blood supply (can lead to hypoxia)

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

What are the different types of hypoxia? (4)

A
  1. hypoxaemic hypoxia
  2. Anaemia hypoxia
  3. Ischaemic hypoxia
  4. Histiocytic hypoxia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the causes of hypoxaemic hypoxia?

A
  1. Reduced inspired pO2 at altitude

2. Reduced absorption secondary to lung disease

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

What is anaemic hypoxia?

A

Decreased ability of haemoglobin to carry oxygen

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

What are the causes of anaemia hypoxia?

A
  1. Anaemia

2. CO poisoning

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

What are the causes of ischaemic hypoxia?

A
  1. Blockage of a vessel

2. Heart failure

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

What is histiocytic hypoxia?

A

The inability to utilise oxygen in cells due to disabled oxidative phosphorylation enzymes

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

What causes histiocytic hypoxia?

A

Cyanide poisoning

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

How does the immune system damage the body’s cells? (2)

A
  1. Hypersensitivity reactions - host tissue is injured secondary to an overly vigorous reaction
  2. Autoimmune reactions - immune system fails to distinguish self from non-self
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Which cell components are most susceptible to injury? (4)

A
  1. Cell membranes
  2. Nucleus - DNA
  3. Proteins
  4. Mitochondria
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is happening at a molecular level in hypoxia when there is reversible injury? (3)

A

Level of oxidative phosphorylation decreases - ATP levels decrease

  1. Na-K pump functioning decreases - Na+ influx and H2O increases -> Cellular swelling
  2. Glycolysis increases - Anaerobic respiration increases lactic acid - pH falls -> clumping of nuclear chromatin
  3. Detachment of ribosomes - protein synthesis decreases - lipid deposition (fatty liver)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What happens at a molecular level in prolonged hypoxia when there is irreversible injury? (4)

A

Increased cytosolic Ca2+ levels activates many enzymes

  1. ATPase - decreased ATP
  2. Phospholipase - membrane digested
  3. Protease - disruption of membrane and cytoskeletal proteins (cell shape changes)
  4. Endonuclease - nuclear chromatin damage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are free radicals?

A

Reactive oxygen species - single unpaired electron in outer orbit (want to gain an electron)

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

Give three examples of free radicals.

A
  1. OH. (hydroxyl)
  2. O2- (superoxide)
  3. H2O2
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Where are free radicals usually locked away in cells?

A

Mitochondria

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

How are free radicals produced? (5)

A
  1. Normal metabolic reactions - oxidative phosphorylation
  2. Inflammation - oxidative burst of neutrophils
  3. Radiation
  4. Contact with unbound metals in the body (iron - haemachromatosis)
  5. Drugs and chemicals (liver’s P450 system
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

How does the body control free radicals? (3)

A
  1. Anti-oxidant system - Vitamins A, C, E ‘neutralise’ them
  2. Metal carrier and storage proteins - eg. transferrin
  3. Enzymes (neutralise them) - eg superoxide dismutase
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

How do free radicals injure cells? (3)

A
  1. Oxidative imbalance
  2. Lipids in cell membranes targeted - causes lipid peroxidation -> autocatalytic chain reaction
  3. Oxidation of proteins, carbohydrates and DNA (mutagenic, carcinogenic)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

How can a cell protect itself against injury?

A
  1. Heat shock proteins - ‘mend’ mis-folded proteins and maintain cell viability
  2. Unfoldases or chaperonins
  3. eg ubiquitin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What do injured and dying cells look like under a light microscope?

A
  • Injured: pale and swollen cytoplasm
  • pyknosis: eosinophilic cytoplasm, clumped proteins
  • karyorrhexis: nucleus broken up into bits
  • karyolysis: nucleus dissolves away
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What does reversible injury look like under an electron microscope? (7)

A
  1. Blebs - cytoskeleton broken down by proteases
  2. Generalised swelling
  3. Clumping of nuclear chromatin
  4. Autophagy by lysosomes (leakiness)
  5. ER swelling
  6. Dispersion of ribosomes
  7. Mitochondrial swelling
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What does irreversible injury look like under an electron microscope? (5)

A
  1. Rupture of lysosomes and autolysis
  2. Nucleus (pyknosis, karyorrhexis or karyolysis)
  3. Lysis of ER
  4. Defects in cell membrane (holes)
  5. Myelin figures
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

How can cell death be diagnosed?

A

Dye exclusion test - cells with the dye in them are dead

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
What is oncosis?
Cell death with swelling - spectrum of changes that occur in injured cells prior to death
26
What is necrosis?
Morphological changes that occur in a living organism after a cell has been dead some time - seen after 12-24 hours
27
What are the different types of necrosis? (4)
1. Coagulative 2. Liquefactive 3. Caseous 4. Fat necrosis
28
What are some characteristics of coagulative necrosis? (2)
1. Ischaemia of solid organs - lots of connective tissue | 2. Protein clumping
29
What are some characteristics of liquefactive necrosis? (4)
1. Loose tissues 2. Presence of neutrophils (infection) 3. Enzyme release (lysosomes) 4. More Destruction rather than clumping
30
What does coagulative necrosis look like?
Cellular architecture somewhat preserved - "ghost outline" of cells
31
What does coagulative necrosis look like under a microscope?
- very pink staining of protein clumps - cant see nuclei properly - karyolysis
32
What is caseous necrosis?
- 'Cottage cheese' appearance - between coagulative and liquefactive necrosis - characteristic of tuberculosis
33
What does fat necrosis look like?
Little drops of wax
34
What is gangrene?
Necrosis visible to the naked eye
35
What is an infarction?
Ischaemic hypoxia results in reduced arterial blood flow (infarction) which leads to necrosis
36
What is an infarct?
Area of necrotic tissue
37
What is dry gangrene?
Coagulative necrosis modified by exposure to air
38
What is wet gangrene?
Liquefactive necrosis modified by infection
39
What is gas gangrene?
Wet gangrene where the infection is with anaerobic bacteria that produce gas
40
What are the causes of infarction?
1. Thrombosis 2. Embolism 3. External pressure on vessels
41
When are infarcts white?
- Mostly in coagulative necrosis - solid organs - occlusion of an end-artery
42
When are infarcts red?
- mainly in loose tissue - dual blood supply - anastomoses - prior congestion - raised venous pressure - reperfusion
43
What is ischaemia-reperfusion injury?
Blood flow returned to damaged tissue results in worse damage than if blood flow wasn't returned
44
What are the causes of ischaemia-reperfusion injury?
1. Increased production of free radicals 2. Increased number of neutrophils - inflammation 3. Delivery of complement proteins
45
Which important substances leak out of cells? (3)
1. Potassium 2. Enzymes 3. Myoglobin
46
What is apoptosis?
Programmed cell death with shrinkage, induced by regulated intracellular program where a cell activates enzymes that degrade it's own nuclear DNA and proteins
47
List the characteristics of apoptosis. (4)
1. Equal and opposite force to mitosis 2. Enzymes activated that degrade nuclear DNA and protein 3. Membrane integrity is maintained 4. Lysosomal enzymes not involved 5. Can be pathological or physiological
48
When does apoptosis occur physiologically? (2)
1. Hormone-controlled involution - ovaries smaller in menopausal women 2. Embryogenesis - cells between fingers-to-be undergo apoptosis
49
When does apoptosis occur pathologically? (3)
1. Cytotoxic T cell killing of virus infected or neoplastic cells 2. Damaged cells (particularly DNA damage) 3. Graft vs host disease (eg bone marrow transplant)
50
Describe the process of apoptosis visually. (4)
1. Normal cell 2. Condensation (shrinking) 3. Fragmentation 4. Apoptotic bodies - budding (equal sized fragments)
51
What are the 3 phases of apoptosis?
1. Initiation 2. Execution 3. Degradation and phagocytosis
52
How do initiation and execution of apoptosis occur?
Intrinsic and extrinsic mechanisms Activation of caspases - control and mediate apoptosis - cause cleavage of DNA and proteins of cytoskeleton
53
What triggers the intrinsic pathway (apoptosis)?
- irreparable damage | - withdrawal of growth factors (eg ovaries in menopause)
54
What happens in the apoptosis intrinsic pathway? (4)
1. Triggered p53 activation 2. outer mitochondrial membrane becomes leaky 3. Mitochondria releases cytochrome C 4. activation of caspases
55
What triggers the apoptosis extrinsic pathway? | How do they trigger this process?
- Cells that are a danger - tumour cells, virus-infected cells - Display proteins on membrane detected by immune cells
56
Why apoptotic bodies express proteins phagocytosed?
- Apoptotic bodies express proteins on their surface | - Recognition by phagocytes or neighbouring cells
57
What are the differences between apoptosis and oncosis? (3)
1. Shrinkage and chromatin condensation (A) vs swelling (O) 2. Budding (A) vs blebbing with disruption of cell membrane (O) 3. No inflammation (A) vs inflammation (O) 4. Single cells (A) vs Contiguous group of cells (O)
58
What happens to a cell's membrane in oncosis and apoptosis?
Oncosis - disrupted, early lysis | Apoptosis - intact
59
When does fluid accumulate in cells?
Energy supplies cut off (eg hydroxia) - Hydropic swelling
60
How does fluid accumulate in cells?
Na+ and water flood into cell
61
Why is fluid accumulation a particular problem in the brain (cerebral oedema)?
Fluid sits in the skull which is a solid 'cage' - limited volume to expand into Blood supply is compromised - increased pressure
62
When do lipids accumulate in cells?
1. Reduced function of liver (major organ of fat metabolism) 2. Cholesterol not able to be broken down and is insoluble - excess stored in vesicles - steatosis (accumulation of triglycerides
63
What are the causes of lipid accumulation in cells?
1. Alcohol (reversible in about 10 days) 2. Diabetes mellitus 3. Obesity 4. Toxins (eg carbon tetrachloride)
64
Where is excess cholesterol accumulated and in which conditions?
- atherosclerotic plaques: smooth muscle cells and macrophages - hereditary hyperlipidaemias: macrophages in skin and tendons (xanthomas)
65
What do accumulated proteins in cells look like?
Eosinophilic droplets or aggregations in the cytoplasm
66
In which conditions do proteins accumulate in cells?
1. Alcoholic liver disease - damaged keratin filaments (Mallory's hyaline) 2. a1-antitrypsin deficiency
67
When do (non-endogenous) pigments accumulate in cells?
- Urban air pollutants - carbon/coal/dust/soot | - tattooing
68
What happens as a result of accumulation of carbon/coal/dust/soot in the lungs? (Explanation + conditions) (4)
- alveolar macrophages phagocytose the particles 1. anthracosis (carbon in lungs) 2. blackened peribronchial lymph nodes (macrophages migrate from alveoli to peribronchial lymph nodes 3. Fibrosis - if in large amounts 4. Emphysema (coal worker's pneumoconiosis)
69
What happens to tattoo pigments that are pricked into the skin?
Phagocytosed by macrophages in dermis and remains there | - some pigment reaches draining lymph nodes
70
Name an endogenous pigment that can be accumulated.
Haemosiderin
71
What is haemosiderin?
Iron storage molecule | - derived from haemoglobin, yellow/brown
72
What can lead to haemosiderin being accumulated?
Systemic or local excess of iron - eg BRUISES
73
In which clinical can haemosiderin be accumulated? (4)
1. Haemosiderosis - systemic overload of iron 2. Haemolytic anaemias 3. Blood transfusion 4. Hereditary haemochromatosis
74
What is hereditary haemochromatosis?
- genetically inherited disorder - results in increased intestinal absorption of dietary iron - iron deposited in skin, liver, pancreas, heart and endocrine organs - often associated with scarring in liver (cirrhosis) and pancreas - 'bronze' diabetes
75
What are the symptoms and treatment of/for hereditary haemochromatosis?
- liver damage - heart dysfunction - multiple endocrine failures - especially of the pancreas - treatment: repeated bleeding
76
What does hereditary haemochromatosis look like to the naked eye?
Very tanned skin
77
What accumulates in jaundice?
Bilirubin
78
What is bilirubin?
Breakdown product of heme, stacks of broken porphyrin rings
79
Where is bilirubin produced?
Bilirubin is formed in all cells of the body because all cells contain cytochromes which contain heme
80
Which carrier protein transports bilirubin in the body? Where is bilirubin transported to?
Albumin transports bilirubin from tissues to liver
81
How does jaundice arise?
When bile flow is obstructed or overwhelmed, bilirubin in blood rises and results in jaundice
82
Where is excess bilirubin deposited? (2)
1. In tissues extracellularly | 2. Macrophages
83
What are the different mechanisms of intracellular accumulations? (4)
1. Abnormal metabolism 2. Alterations in protein folding and transport 3. Substrate build-up - deficiency of critical enzymes 4. Inability to degrade phagocytosed particles
84
Where does dystrophic (local) calcification occur? (4)
1. Area of dying tissue 2. Atherosclerotic plaques 3. Aging or damaged heart valves 4. Tuberculous lymph nodes
85
Why does dystrophic calcification occur?
A local change or disturbance in the tissue favours the nucleation of hydroxyapatite crystals
86
Which type of calcification occurs due to abnormality in calcium metabolism or serum calcium or potassium concentrations?
Metastatic
87
Why does metastatic calcification occur?
Due to hypercalcemia secondary to disturbances in calcium metabolism - increased secretion of parathyroid hormone or destruction of bone
88
What causes hypercalcaemia?
1. Increased secretion of parathyroid hormone (PTH) resulting in bone resorption 2. Destruction of bone tissue
89
Which cells can replicate indefinitely?
Germ cells
90
Why can germ cells replicate indefinitely?
They contain telomerase - maintains the original length of telomeres

ESA 2 - Pathological Processes (4 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions