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Pathology I > Mechanisms Of Cell Injury > Flashcards

Mechanisms Of Cell Injury Flashcards

1
Q

Describe cell injury.

A

-disruption of cell homeostasis or steady state
-injury from outside/inside cell
-affects 1 or more imp cell structure
-resp of cell to injury:
>adaptation
>degen
>death of cell
-reversible -> healing
-irreversible -> degen or death

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2
Q

Describe the morphology of cell injury.

A

Depends on:
-what caused the injury
-extent of injury
-duration of injury
-cell type affected

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3
Q

Describe the causes of cell injury.

A

MOST COMMON:
>oxygen deficiency
>infectious agents common/imp
>immunological dysfunction
-workload imbalance: atrophy, hyperplasia, hypertrophy, metaplasia
-physical agents: heat, cold, crush, friction, UV rad, electrocution
-nutritional imbalance: cal deficiency/excess, vit/mineral deficiency/excess
-genetic derangement: esp selective breeding
-toxins
-aging

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4
Q

Describe oxygen deficiency.

A
  1. Hypoxia = partial reduction in O2 delivery to a tissue
  2. Anoxia = no O2 delivery to a tissue
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5
Q

Describe what causes hypoxia/anoxia.

A
  1. Inadequate oxygenation of blood
    -heart failure
    -respiratory failure
  2. Reduced transport of O2 in blood
    -anemia
    -CO toxicosis
  3. Reduction in blood supply = ischemia
    -thrombosis
    -ex: feline aortic thromboembolism ‘saddle thrombus’ (secondary to hypertrophy cardiomyopathy) causes anoxic damage to hind limbs
  4. Blockage of cell respiratory enzymes
    -cyanide toxicosis
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6
Q

Describe infectious agents.

A
  1. Viruses
    -obligate intracellular parasites -> use host cell enzyme system
    -cell survival depends on method viruses leave the cell
  2. Bacteria
    -toxins
    -uncontrolled replication
  3. Fungal (mycosis)
    -progressive, chronic inflammatory disease
  4. Protozoan
    -replicate in specific host cells -> cell destruction
  5. Metazoan parasites (nematode/cestodes)
    -inflammation, tissue distortion, utilization of host nutrients
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7
Q

Describe immune dysfunction.

A
  1. IS fails to respond
    -congenital defects: severe combined immunodeficiency (SCIDS, Arabian foals) -> antigen receptors (lymphocytes)
    -acquired defects (AIDS/HIV)
    >can be transient
    —results from damage to lymphoid tissue
    —viral infections, chemicals, drugs
  2. IS over respond or aberrant reaction
    -autoimmune disease
    -hypersensitivity reaction
    >anaphylaxis, FAD, feline asthma
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8
Q

Describe how workload imbalance can lead to cell adaptation.

A
  1. Compensation
    -inc workload = hypertrophy, hyperplasia
    -dec workload = atrophy, oncotic
  2. Cant compensate
    -degen & poss death
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9
Q

Describe the 6 mechanisms of cell injury.

A
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10
Q

Describe depletion of ATP.

A

made thru 2 primary metabolic pathways:
1. Aerobic: Krebs cycle
Glu + oxygen -> CO2 + H2O + energy (2900 kJ/mol)
2. Anaerobic: glycolysis
Glu + lactic acid + energy (120 kJ/mol)
both require glu
-ATP needed for almost all synthetic & degradative processes within the cell
-culminates irreversible mitochondrial & lysosomal membrane damage -> cell necrosis

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11
Q

Describe what happens when depletion of ATP is 5%-10%.

A
  1. Na/K ATPase pump fail
    -cell swell
    -ER swell
    -PM damage
  2. Altered cell metabolism
    -anaerobic glycolysis
    >deplete glycogen stores
    >inc lactic acid -> dec pH -> loss of enzyme function
  3. Ribosome detachment
    -dec protein syn
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12
Q

Describe mitochondrial injury.

A
  1. Formation of mitochondrial permeability transition pore (MPTP)
    -high conductance channel in mitochondrial membrane
    -opened = loss of membrane potential
    >failure of oxidative phosphorylation
    >progressive depletion of ATP
    >cell necrosis
  2. Inc prod of reactive oxygen species (ROS)
  3. Activation of apoptotic pathways
    -proteins activate apoptosis pathway in mitochondria
    -leakage of apoptosis activating proteins into cytosol -> cell death
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13
Q

Describe loss of Ca homeostasis - accumulation of Ca2+ sources (3).

A
  1. Extrinsic (cell damage)
  2. Intrinsic: SER & mitochondria
    *sets off cascade of events
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14
Q

Describe the accumulation of Ca cascade of intracellular events.

A
  1. Opening of MPTP = dec ATP
  2. Enzyme activation
    -phospholipases: membrane damage
    -proteases: membrane & cytoskeleton proteins
    -endonucleases: DNA & chromatin fragmentation
    -ATPases: break down ATP, accelerate ATP depletion
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15
Q

Describe the accumulation of Ca 3 major forms of damage.

A
  1. Membrane damage
  2. Nuclear damage
  3. ATP depletion
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16
Q

Describe reactive oxygen species (ROS).

A

-from oxygen
-made during cell respiration by mitochondria
-molecules/atoms w unpaired elections = reactive free radical
-cell quenching/scavenging system neutralize normally
-excess ROS or dec scavenging capacity = oxidative stress -> damage lipid, protein, DNA

17
Q

Describe the normal metabolic processes of ROS.

A

-reduction oxygenation reactions
(O2 + 2H2 -> 2 H2O)
-transfer of 4 e-
-sm amt of partially reduced intermediated made
1. Superoxide anion (O2-) 1e-
2. Hydrogen peroxide (H2O2) 2e-
3. Hydroxyl ions (-OH) 1e-

18
Q

Describe the pathological sources of ROS.

A
  1. Inflam
    -rapid burst of ROS made by activated WBC (neutrophil) -> gen superoxide anion (O2-)
  2. Transition metals (iron, copper)
    -donate/accept free e-
    -catalyze free radical formation
  3. Nitric oxide (NO)
    -imp chemical mediator
    -gen by endothelial cells, macrophages, neurons
    -act as free radical
    -converted into peroxynitrite anion ONOO-, NO2, NO3
  4. Absorption of radiant energy
    -H2O + ionizing radiation -> -OH + H
  5. Oxidative stress
    -cell injury
    -cancer
    -aging
    -degen disease
19
Q

Describe neutralization of ROS/removal of free radicals.

A
  1. Spontaneous decay
    -(O2- + H2O -> O2 + H2O2)
  2. Enzymes
    -catalase, superoxide dismutase, glutathione peroxidase
    >break down H2O2 & O2
    >near sites where oxidants formed
  3. Storage & transport proteins
    -transferrin, ferritin, ceruloplasmin
    -bind reactive metals like Fe & Cu
  4. Antioxidants (VitE & A, glutathione)
    -block initiation
    -inactivate (scavenge)
20
Q

Describe the pathological effects of ROS.

A
  1. Lipid peroxidation in membranes -> membrane damage
    -formation of peroxides -> autocatalytic reaction (propagation)
    >dec phospholipid syn
    >inc phospholipid breakdown
    >cytoskeletal abnormalities
    -activation of proteases -> damaged cytoskeleton
    -cell stretch & rupture
  2. Oxidative modification of proteins -> damage active sites, change conformation, enhance degradation
    -gen by monamine oxidase (MOA) in outer mitochondrial membrane
    -PM damage (loss of osmotic balance)
    -injury to lysosomal membrane (leak enzyme into cytoplasm & enzymatic digestion)
  3. Lesions in DNA -> cell aging, malignant transformation, mutation
    -MOA
21
Q

Describe membrane damage mechanisms.

A
  1. ROS
  2. Dec phospholipid syn: secondary to defective mitochondrial function/hypoxia
    -dec prod of ATP -> dec phospholipid syn
    -affect all cell membrane
  3. Inc phospholipid breakdown
    -activate Ca dependent phospholipases
    -accumulate lipid breakdown products
    >detergent effect on membrane
    >insert into membranes
    —changes in permeability & electrophysiologic alterations
22
Q

Describe the cytoskeletal abnormalities of membrane damage.

A

-Inc cytosolic Ca -> activate proteases -> damage cytoskeleton
-in presence of swelling = PM can detach from cytoskeleton -> sus to stretching & rupture

23
Q

Describe the summary of membrane damage.

A

-dec O2 & inc cytosolic Ca in ischemia or ROS cause membrane damage

24
Q

Describe the consequences of membrane damage.

A
  1. Mitochondrial membrane damage
    -open MPTP -> leak pro apoptotic proteins
    -dec ATP
  2. PM damage
    -loss of osmotic balance -> influx of fluids & ions
    -loss of cell contents & metabolites
  3. Injury to lysosomal membranes
    -leak enzymes into cytoplasm: RNases, DNases, proteases, phosphatases, glucosidases
    -enzymatic digestion of RNA, DNA, proteins
25
Q

Describe the clin path of membrane damage.

A

-chem panels used to determine hepatocellular injury
-alanine aminotransferase (ALT)
>located in cytoplasm of hepatocytes
>converts alanine -> pyruvate
>pyruvate used for gluconeogenesis or Krebs cycle
-when hepatocytes have cell injury ALT is released
>cell necrosis
>membrane blebs w ALT

26
Q

Describe protein damage.

A

-misfolded proteins
>mutation
>free radical damage
-repair mech overwhelmed -> protein in ER -> ER stress -> apoptosis

27
Q

Describe DNA damage: repair, apoptosis, senescence, cancer.

A

-radiation, cytotoxic anticancer drugs, hypoxia
>direct damage
>free radical damage
-repair mech overwhelmed -> initiate apoptosis

Pathology I (17 decks)

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