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Path300 > Adaptation, Injury & Cell Death > Flashcards

Adaptation, Injury & Cell Death Flashcards

1
Q

How do cells adapt to a stressor (5)?

A 
Atrophy
Hyperplasia
Hypertrophy
Metaplasia
Dysplasia
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2
Q

What are the causes of atrophy (5)?

A

Decrease workload
« » neuronal stimulation
« » hormonal « »

Insufficient blood flow
« » nutrition

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3
Q

How atrophy occur (mechanism)?

A

Decrease in prot synthesis
Increase PROT DEGRADATION

Or AUTOPHAGY
Ingest its own organelles (attempt to conserve energy and survive)

Eg.: lack of nutrients activates UBIQUITIN ligase (E3) to attach multiple ubiquitin mol onto unnecessary prots.

Prots w/ attached ubiquitin mols are transported towards PROTEASOMES.

Proteasome job: degrade prots & recycles aa

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4
Q

In atrophy, which pathway is use for the degradation of prots?

A

Ubiquitin-proteasome pathway

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5
Q

What are the causes of hypertrophy (2)?

A

Increase workload

« » hormonal stimulation (growth factor, anabolic steroids)

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6
Q

What are the 2 types of hypertrophy and explain it

A

Physiological = n d/t increase demand

Pathological = compensatory following a disease (eg.: myocardial infarct)

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7
Q

How hypertrophy occurs (mechanism) (3)?

A

Increase prot and cell synthesis
Optimization of cell fct
Enzymatic induction (liver)

Optimization: muscle hypertrophy, some myosin chains are replaced by more energetically efficient chains.

Increase metabolism via 
MECHANICAL: stress
TROPHIC: growth factor
Trigger induce gene transcription 
Induce prot/c synthesis
Increase functionnality
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8
Q

Give an example of hypertrophy of functional enzymes (enzymatic induction in the liver).

A

Chronic alcoholics

Become + tolerant to higher dose of alcohol
Because they have a GREATER NMB of liver ENZYMES & they work FASTER

Liver enzymes: responsible for breakdown and metabolism of alcohol.

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9
Q

What is the difference b/w pathological hyperplasia and cancer?

A

Hyperplasia occurs in response to ABNORMAL STIMULUS
It STOPS if the stimulus is REMOVED

Cancer: proliferation despite absence of stimulus

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10
Q

What is metaplasia?

A

A substitution of cell from one type to another.

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11
Q

Give an example of metaplasia

A

Substitution of normal COLUMNAR epithelium into SQUAMOUS metaplasia in airways of SMOKERS

(From ciliated to squamous)

Squamous cells: survival advantage in presence of smoke
BUT
Decrease in ciliary mvt increase ACCUMULATION of TOXIC particles in the lung

Cause LUNG CANCER in long term

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12
Q

How metaplasia occur (mechanism)

A

Reprogramming of STEM CELLS to differentiate into a different phenotype.

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13
Q

What is dysplasia?

A

Metaplasia cells w/ ABNORMAL structure and fct

New fct can be unrelated to any of the know cell types

If exposed for a long time to a stressor CAN become PERMANENT

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14
Q

What part of the cell are more vulnerable to cell injury (5)?

A

Mitochondria

Plasma membrane

ER

Protein synthesis

Nucleus/DNA

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15
Q

What type of cells are more vulnerable to ischemia?

A

Neurons

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16
Q

What are the major causes of cell injury(9)? Pense aux cours de la session jusqu’à présent

A

Hypoxia

Free radical

Physical

Chemical

Biological

Immune reactions

Genetic abnormalities

Nutritional imbalance

Aging

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17
Q

What is hypoxia?

A

Oxygen deficiency

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18
Q

Define ischemia

A

Inadequate blood supply to cells

Major cause of hypoxia

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19
Q

Name 4 causes of ischemia

A

Atherosclerosis

Thrombus
Embolism

Vessel spasm

Compression

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20
Q

Name 2 types of cell death d/t ischemia

A

Myocardial infarct

Stroke

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21
Q

Name 3 types of hypoxia caused by poor oxygenation of the blood

A

Severe anemia

Carbon monoxide poisoning

Pneumonia

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22
Q

Explain the mechanism of hypoxic injury

A

Decrease of 02
Decrease ATP prod (via oxidative phosphorylation)

Voir p.10

23
Q

Severe ischemia lead to which ion influx?

A

Calcium

24
Q

In severe ischemia calcium influx activates which enzymes?

A

ATPase

Protease

Phospholipase

Nuclease

Damage plasma membrane/nuclear membrane (d/t an increase in phospholipid & membrane prot breakdown)

If cell dies = necrosis

25
Q

Free radicals react with what (3)?

A

Nucleic acid

Lipid

Prots

26
Q

Free radicals initiate the formation of what?

A

More free radicals

27
Q

What is a free radical?

A

Very reactive molecule w/ unpaired electrons

2nd most common cause of cell injury

28
Q

Free radical cell injury is common in what case?

A

Ischemic reperfusion

Huge prod of ROS when blood supply is restored after being depleted for a while because c is OVERCOMPENSATING

29
Q

What is the major free radical in cell injury?

A

Reactive oxygen species (ROS)

Eg.: superoxide anion 02•-

30
Q

How ROS is produce naturally and give 2 examples?

A

Prod via REDOX REACTION
Such as
Mitochondrial resp
Within lysosome of immune cells

Mitochondrial damage=high amount of ROS released

Also 
Radiation
UV light
Chemical agents (cigarette smoke)
Inflammation
31
Q

Name enzymes and antioxidants that regulate ROS

A

Enzyme
Superoxide dismutase (SOD)
Glutathione peroxidase (GSH)
Catalase

Antioxidants
Vit A E C
B-carotene
(free radical scavengers)

32
Q

Explain the 3 mechanism of ROS injury

A
  1. LIPID PEROXIDATION of membrane
    - membrane damage
    - blebs
    - formation of more ROS
  2. PROTS DAMAGE
    - breakdown
    - misfolding
  3. DNA DAMAGE
    - mutation leading to cancer
    - cell death
    - aging

If cell dies=necrosis

33
Q

Give examples of physical injuries (3)

A

Trauma

Electric shock

Extreme temperatures

34
Q

Give example of what causes chemical injuries (6)

A

Polluants

CO

Insecticides

Asbestos

Ethanol

Therapeutic drugs

35
Q

Explain how a chemical injury injured cells

A

Alter
Integrity of plasma membrane
Osmotic homeostasis
Enzymatic/prot fct

36
Q

Explain how biological agents cause cell injury

A

Replication
Secreted toxins
Impair w/ normal tissue fct/metabolism

Bacteria
Viruses
Worm

37
Q

Give example of immune reaction that can cause cell injury (2)

A

Autoimmune disease
Allergic reactions
-complement cascade
-cell-mediated toxicity

38
Q

Give examples of genetic abnormalities that can cause cell injuries (4)

A

Sickle cell anemia

Down syndrome

Huntingdon’s disease

Spinal muscular atrophy

39
Q

Explain how genetic abnormalities can cause cell injuries (3)

A

Damage d/t

Impaired prot fct
Accumulation of misfold prot
DNA mutations

40
Q

Define polymorphism

A

Genetic variant
Can predispose to certain injury
Or
Dev of diseases

41
Q

Give an example of polymorphism

A

Albino’s more vulnerable to UV light damage

42
Q

What are the risks associate with the accumulation of cell injury/ impaired metabolism d/t nutritional imbalances (3)?

A

Increase risk of

Infections

Db

Heart diseases

43
Q

Explain what is cellular senescence

A

Alteration in replicative capabilities of cells

  • diminished adaptation
  • increased cell death
44
Q

Name the different types of necrosis (4)

A 
COAGULATION
Scar tissue (eg.: fibroblasts) to avoid having a hole

LIQUEFACTIVE
Leave a hole

CASEOUS
B/w solid/liquid
Mix of hole & scar tissues

GANGRENE
Coagulative + bacterial infection

45
Q

Give examples for each types of necrosis

Coagulation

Liquefactive

Caseous

Gangrene

A

Coagulation = myocardial infarct

Liquefactive = abscess lung/brain

Caseous = tb

Gangrene = severe frostbites/ischemia

46
Q

When does apoptosis occurs?

A

Tissue turnover

Injury

  • DNA/prot damaged beyond repair
  • deprived of growth factor
47
Q

Give examples of apoptosis

A

Skin shredding

Lining of GIT turnover

Delayed damage to spinal cord

48
Q

What part of the cell released factor promoting or inhibiting apoptosis?

A

Mitochondria

49
Q

What can trigger extrinsic apoptosis?

A

Viruses
Immune cells
Radiation
Mitochondrial content

50
Q

How cytotoxic t cells kills infected cells?

A

Via apoptosis

Death receptor (extrinsic) pathway

51
Q

In what disease is there a high concentration of caspase?

A

Neurodegenerative diseases

52
Q

What causes intracellular accumulation (3)?

A

Ineffective removal

Inability to remove d/t genetic disease or lack of enzyme

Unable to store

53
Q

Give examples of intracellular accumulation (5)

A

SILICIA
Accumulation in the lung of minors

PIGMENTS
Tattoos

MELANIN
Accumulation in freckles

CALCIUM
Heart valves

LIPOFUSCIN
Not harmful
Marker of past free-radical injury/aging/atrophy
(Common in heart/brain/liver)

Path300 (12 decks)

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