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Medical school year one week one > Cell pathology lecture 2-3 > Flashcards

Cell pathology lecture 2-3 Flashcards

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USMLE® Step 1 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
Q

What is paracrine communication?

A

Another cell in the viscinity signals a cell. Growth factors can act via this way

26
Q

What does endocrine mean

A

A mediator is released into the bloodstream, travelling to a distant target. Includes FSH

27
Q

What are the signals cells respond to?

A

Pathogens, damage to neighbouring cells, contact with neighbouring cells, contact with extracellu;ar matrix, secreted molecules such as growth factors, cytokines or hormones

28
Q

What happens once a ligand binds to a receptor?

A

An ion channel can open
A G-protein is activated
Tyrosine kinase can activate
or latent transcription factor can activate

29
Q

What are G-protein receptors?

A

They trigger G-proteins which are attached to inner aspect of membrane, triggering a response

30
Q

What does p53 do

A

it is a transcription factor activating genes causing growth arrest

31
Q

What are the 5 possible purposes of growth factors

A

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
Q

What does the extracellular matrix do?

A

Support anchorage, polarity and migration,
Controls cell proliferation via growth factors and integrin signalling,
Scaffolding for tissue nenewal, estabishment of tissue microenvironments

33
Q

What makes up the extracellular matrix?

A

Collagen and elastin for structure, proteoglycans and glycoproteins

34
Q

What are the stages of the cell cycle?

A

G1 (duplicates organelles, chromosome replication begins)
S (DNA replicated)
G2 (Growth continues, enzymes and other proteins, chromosome replication continue)
Mitosis

35
Q

What are totipotent stem cells?

A

They can differentiate to all cell types

36
Q

What tissues can adult stem cells replace

A

Only the tissue in which they reside

37
Q

What are the two important properties of stem cells?

A

Self renewal and asymmetric division (2 daughter cells, one a replica, the other can differentiate)

38
Q

What can damage cells?

A

Oxygen deprivation, physical agents, chemicals/drugs, infectious agents, immune reactions, genetic abnormalities, nutritional imbalances

39
Q

What cell injuries are reversible?

A

Cell swelling, fatty change, eosinophilia, cell membrane blebbing, mitiochondiral swelling, dilation of ER with ribosome detatchment, chromatin clumping

40
Q

What is hypertrophy?

A

Increase in size of cells, increasing size of organ. Pathological (myocardium in hypertension) or physiological (Muscle, uterus), increased workload

41
Q

What is hyperplasia?

A

Increase in number of cells in response to stimulus. Can be pathological or physiological

42
Q

What is atrophy?

A

The reduction in organ size/tissue due to decrease in cell size and number (eg uterus post birth)

43
Q

What are the 6 types of pathological atrophy

A

Disuse, denervation, diminished blood suppky, inadequate nutrition, loss of endocrine stimulation, pressure

44
Q

What is metaplasia?

A

A reversible change where one differentiated cell type is replaced by another type

45
Q

What can squamous cells differentiate to in lower oesophagus in response to acid reflux?

A

Goblet cells

46
Q

What are the 3 outomes of a cell following irreversible injury?

A

Necrosis, apoptosis, necroptosis + pyroptosis

47
Q

What is necrosis?

A

Unregulated cell death with lysosomal enzyme digestion of membranes and cell leakage. Inflammatory

48
Q

What causes necrosis?

A

Infection, ischaemia, toxins, trauma

49
Q

What mechanisms underly cell imjury in necroisis?

A

ATP depletion, mitochondiral damage, influx of calcium, oxygen derived free radicals, membrane permeability defects, DNA and protein damage.

50
Q

What does an influx of calcium do in cells?

A

activates enzymes destroying cell, Opens mitochondrial permeability transition pores: depletes ATP

51
Q

What is apoptosis

A

Highly regulates, programmed cell death caused by protein/DNA damage. No loss of membrane integrity or inflammation

52
Q

What occurs in apoptosis

A

Cell shrinkage, chromatin condensation, formation of apoptotic blebs and apoptotic antibodies, phagocytosis by macrophages.

53
Q

What is the intrinsic mitochondiral pathway of apoptosis?

A

Cellular injury, DNA damage or decreased hormona; stimulation inactivates BCL2, allows cytochrome C to activate caspases. Caspase 9 initiates

54
Q

Describe the extrinsic receptor-ligand pathway of apoptosis

A

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
Q

What molecule flips from inner to outer membrane to be recognised by macrophages?

A

Phosphatidylserine

Medical school year one week one (6 decks)

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