Cell pathology lecture 2-3 Flashcards

1
Q

What is homeostasis?

A

The way internal variables are kept in a normal range

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2
Q

Give the order of negative feedback

A

Stimulus->variable->receptor senses change ->Control centre compares to normal value -> Effectors make adjustments against reference value ->effectors make variable normal

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3
Q

List some of the determinants of cell viability:

A

Protection from environment, nutrition, communication, energy generation, movement, renewal of senescent/old molecules, molecular catabolism

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4
Q

What are the purposes of the mitochondria?

A

ATP generation, source of intermediates for metabolism, haem production, apoptosis regulators

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5
Q

What is the warburg effect

A

Cancer cells do not break down sugar completely, only completing glycolysis

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6
Q

What do cell membrane proteins & glycoproteins do?

A

Ion & metabolite transport,
Fluid phase & receptor mediated uptake of macromolecules,
Cell ligand, cell matrix and cell-cell interactions

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7
Q

What molecules can move though membranes by passive diffusion?

A

Oxygen, Carbon dioxide, water, urea, alcohol, steroids

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8
Q

How does water move passively?

A

Via osmosis

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9
Q

What causes water to move into/out of cells?

A

High extracellular salt: water goes into cells. Hypotinic extracellular: Water comes out

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10
Q

How do polar molecules >75 daltons and ions move across membranes?

A

Channel (fast) proteins or carrier (slower) proteins

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11
Q

what is needed for passive transport?

A

A concentration gradient

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12
Q

What are the 2 types of endocytosis and which is vitamin uptake done by?

A

Caveolae mediated and receptor mediated (Vitamin is caveolae)

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13
Q

What is transcytosis?

A

Movement of endocytosed vesicles between basolateral and apical aspects of the cell.

Involved in vessel wall permeability, movement of antibodies from breast milk though babys intestinal cells

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14
Q

What is an example of receptor-mediated endocytosis?

A

LDL cholestero luptake

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15
Q

WHat are the four main components of the cytoskeleton

A

Actin microfilaments, intermediate filaments, microtubules, lamin

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16
Q

What joins adjacent cells?

A

Desmosomes

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17
Q

What joins cells to epithelial matrix?

A

Hemi-desmosomes

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18
Q

What makes rough ER rough?

A

It is studded with ribosomes

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19
Q

What does sER do?

A

Cyclical release and storage of calcium ions for muscle contraction

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20
Q

What happens in Endoplasmic reticulum itself?

A

Proteins fold

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21
Q

What are lysosomes and proteosomes involved in?

A

Waste disposal. Lysosomes contain acid hydrolases, proteosomes recycle senescent or misfolded proteins

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22
Q

How do mitochondia mediate cells

A

Mediate oxidative phosphorylation. Rapidly growing cells do this very quickly

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23
Q

What occurs in the intermembrane space of mitochondia?

A

ATP synthesis

24
Q

What is autocrine communication?

A

sending the message to the own cell, occurs during cell development or to amplify a response

25
What is paracrine communication?
Another cell in the viscinity signals a cell. Growth factors can act via this way
26
What does endocrine mean
A mediator is released into the bloodstream, travelling to a distant target. Includes FSH
27
What are the signals cells respond to?
Pathogens, damage to neighbouring cells, contact with neighbouring cells, contact with extracellu;ar matrix, secreted molecules such as growth factors, cytokines or hormones
28
What happens once a ligand binds to a receptor?
An ion channel can open A G-protein is activated Tyrosine kinase can activate or latent transcription factor can activate
29
What are G-protein receptors?
They trigger G-proteins which are attached to inner aspect of membrane, triggering a response
30
What does p53 do
it is a transcription factor activating genes causing growth arrest
31
What are the 5 possible purposes of growth factors
Stimulate activity of proteins needed for cell survival/growth/division, Promote cells to enter cell cycle, relieve blocks on cell cycle progression, prevent apoptosis, enhance systhesis of cell components
32
What does the extracellular matrix do?
Support anchorage, polarity and migration, Controls cell proliferation via growth factors and integrin signalling, Scaffolding for tissue nenewal, estabishment of tissue microenvironments
33
What makes up the extracellular matrix?
Collagen and elastin for structure, proteoglycans and glycoproteins
34
What are the stages of the cell cycle?
G1 (duplicates organelles, chromosome replication begins) S (DNA replicated) G2 (Growth continues, enzymes and other proteins, chromosome replication continue) Mitosis
35
What are totipotent stem cells?
They can differentiate to all cell types
36
What tissues can adult stem cells replace
Only the tissue in which they reside
37
What are the two important properties of stem cells?
Self renewal and asymmetric division (2 daughter cells, one a replica, the other can differentiate)
38
What can damage cells?
Oxygen deprivation, physical agents, chemicals/drugs, infectious agents, immune reactions, genetic abnormalities, nutritional imbalances
39
What cell injuries are reversible?
Cell swelling, fatty change, eosinophilia, cell membrane blebbing, mitiochondiral swelling, dilation of ER with ribosome detatchment, chromatin clumping
40
What is hypertrophy?
Increase in size of cells, increasing size of organ. Pathological (myocardium in hypertension) or physiological (Muscle, uterus), increased workload
41
What is hyperplasia?
Increase in number of cells in response to stimulus. Can be pathological or physiological
42
What is atrophy?
The reduction in organ size/tissue due to decrease in cell size and number (eg uterus post birth)
43
What are the 6 types of pathological atrophy
Disuse, denervation, diminished blood suppky, inadequate nutrition, loss of endocrine stimulation, pressure
44
What is metaplasia?
A reversible change where one differentiated cell type is replaced by another type
45
What can squamous cells differentiate to in lower oesophagus in response to acid reflux?
Goblet cells
46
What are the 3 outomes of a cell following irreversible injury?
Necrosis, apoptosis, necroptosis + pyroptosis
47
What is necrosis?
Unregulated cell death with lysosomal enzyme digestion of membranes and cell leakage. Inflammatory
48
What causes necrosis?
Infection, ischaemia, toxins, trauma
49
What mechanisms underly cell imjury in necroisis?
ATP depletion, mitochondiral damage, influx of calcium, oxygen derived free radicals, membrane permeability defects, DNA and protein damage.
50
What does an influx of calcium do in cells?
activates enzymes destroying cell, Opens mitochondrial permeability transition pores: depletes ATP
51
What is apoptosis
Highly regulates, programmed cell death caused by protein/DNA damage. No loss of membrane integrity or inflammation
52
What occurs in apoptosis
Cell shrinkage, chromatin condensation, formation of apoptotic blebs and apoptotic antibodies, phagocytosis by macrophages.
53
What is the intrinsic mitochondiral pathway of apoptosis?
Cellular injury, DNA damage or decreased hormona; stimulation inactivates BCL2, allows cytochrome C to activate caspases. Caspase 9 initiates
54
Describe the extrinsic receptor-ligand pathway of apoptosis
FAS ligand binds to CD95 receptor on target cell, activating caspases. TNF binds to receptor to do the same, Caspases 8 and 10 initiate
55
What molecule flips from inner to outer membrane to be recognised by macrophages?
Phosphatidylserine