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BMS test 2 > Path 1 > Flashcards

Path 1 Flashcards

1
Q

What is a reversible cell injury?

A

a cell/tissue has been stressed, but overcomes this stress and resumes normal physiologic function

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2
Q

what is an irreversible cell injury?

A

a cell/tissue has become damaged and will eventually die due to the severity of the damage

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3
Q

what is adaptation?

A

there is a change in cellular tissue structure or function that is almost always due to long-term stresses

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4
Q

what is hypoxia?

A

have a lower level of oxxygen so you don’t have enough oxygen going to your blood or muscles

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5
Q

what is ischemia?

A

you don’t have enough blood supply that would bring in the oxygen and nutrients to meet the metabolic demand

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6
Q

what are DNA and nuclear “disruption”

A
  • karyollysis - chromatin fades
  • pyknosis - chromatin condenses, more basophilic, nucleus shrinks
  • karyorrhexis - nucleus fragments
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6
Q

what are the 2 major cell death categories

A

necrosis and programmed cell death

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7
Q

what is necrosis?

A
  • The agents that have injured the physiology/biochemistry of the cell -> immediate loss of cellular viability
  • If cellular signaling is involved in this process, it is disorganized and unregulated
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8
Q

what is programmed cell death

A
  • Cell death is delayed and requires protein synthesis
  • Cellular signaling is always involved and the cell proceeds through an orderly series of steps -> death
  • This can be due to long-term, irreparable cellular damage or loss of cell use
  • Best examples: apoptosis and necroptosis
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9
Q

what happens when there is a reduction in ATP levels?

A
  • Na+/K+ pump dysfunction and swelling
    ○ Eventually leads to membrane damage
  • Anaerobic metabolism decreases pH (lactic acid, inorganic phosphate)
  • Increased production of free radicals
  • Failure of calcium pumps
    Reduction in protein synthesis, detachment of ribosomes, misfolding of proteins
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10
Q

what happens when there is a high concentration of calcium in the cytosol? (calcium accumulation)

A

○ Activate a variety of destructive enzymes
○ Directly activate caspases
○ Cause calcium release from mitochondria

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11
Q

mitochondrial membranes can be damaged by what?

A

free radical attack

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12
Q

what is the result to lipid breakdown in the phospholipids?

A
  • leaky membranes
  • lipid breakdown products that can have detergent effect on cellular membranes
    § Detergent-like effects:
    □ Unesterified free fatty acids
    □ Acyl carnitine
    ——- -Lysophospholipids
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12
Q

how are free radicals generated?

A
  • normal metabolic processes: oxidation reactions during cellular respiration
  • metabolism of drugs or toxins:
    ○ Acetaminophen, alcohol are good examples
    ○ Radiation - UV light, X-ray
    ○ Fenton reaction - metals receive or donate electrons (copper, iron)
    ○ Leukocytes - to kill pathogens in inflammatory reactions
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13
Q

what is the Fenton reaction?

A

conversion of free iron from Fe3+ state to Fe2+ form

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14
Q

what are some mechanisms to remove free radicals?

A
  • Antioxidants: i.e. Vitamin A, C, E
  • Enzymes
    ○ Catalase - breaks down H2O2
    ○ Superoxide dismutase - converts Ox- to H2O2
    ○ Glutathione peroxidase - decomposes H2O2
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15
Q

what are the physiologic causes of apoptosis?

A
  • Programmed destruction of cells during embryogenesis
    ○ The embryo forms many structures that are no longer required in the fetus
  • Hormone-dependent involution in adult
    ○ Endometrial cell breakdown during the menstrual cycle
    ○ Ovarian follicular atresia in menopause
    ○ Regression of lactating breast after weaning
    ○ Prostatic atrophy after castration
  • Cell deletion in proliferating cell populations
    ○ Intestinal crypt epithelia in order to maintain a constant number
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16
Q

what are the causes of apoptosis as a response to pathology

A
  • death of host cells that served their purpose
  • elimination of potentially harmful self-reactive lymphocytes
  • cell death induced by cutotoxic T cells
  • cell death produced by a variety of innjurious stimuli
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17
Q

when does pathological apoptosis occurs?

A
  • accumulation of misfolded proteins
  • pathologic atrophy/involution of secretory tissues in parenchymal organs
  • pancreas, parotid, kidney
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18
Q

what are the 2 basic stages of apoptosis?

A

initiation and execution

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19
Q

what is the initiation stage of apoptosis?

A

the sequence of events involving recognition of apoptotic signals or cellular damage and activation of intracellular “initiator” caspases

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20
Q

what is the execution stage of apoptosis?

A

“executioner” caspases are activated by the “initiator” caspases and cause the cellular changes of apoptosis

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21
Q

what are the 2 major types of apoptosis?

A

intrinsic pathway and extrinsic pathway

22
Q

the intrinsic pathway for apoptosis results from

A

cellular damage or from lack of growth factors

23
Q

what are Bcl-2, Bcl-X, and Mcl-1 and what do they do?

A

they are anti-apoptotic and they prevent mitochondrial pore formation and leakage of cytochrome c and other pro-apoptotic proteins into the cytosol

24
Q

bax and bak are…

A

pro-apoptotic which form channels in the mitochondria and allow leakage of their contents

25
Q

what increases Bim, Bad, Bid, Puma, and Noxa

A
  • ER stress
  • lack of growth signals
  • DNA damage
26
Q

what activates the mitochondrial leak channel (Bax/Bak)?

A
  • lack of BH4 molecules
  • BH3-only molecules
27
Q

what happens if you open the mitochondrial leak channel?

A
  • Cytochrome C leaks into the cytosol
  • Cytochrome C directly activates a protein known as apoptosis activating factor (APAF) -> activation of caspases
28
Q

how is extrinsic pathway of apoptosis initiated?

A

initiated by activation of plasma membrane death receptors on a variety of cell (Fas receptor)

29
Q

what is the death receptor?

A

Fas receptor

30
Q

what expresses the fas ligands?

A

the T cells that recognize self antigens and some cytotoxic T cells

31
Q

what is formed when the FasL binds to Fas?

A

Fas-associated death domain

32
Q

what does Fas-associated death domain activate?

A

caspases 8 and 10

33
Q

both intrinsic and extrinsic pathways converge in the ?

A

execution phase

34
Q

caspases 8,9, and 10 can all activate

A

executioner caspases

35
Q

executioner caspases can:

A
  • cause cleavage of DNA
  • destroy the nuclear matrix
  • cause cytoskeletal changes
  • activated flippases
36
Q

what is the end result of the execution phase?

A
  • DNA is cut into discrete lengths by endonucleases activated by caspases
  • Phosphatidylserine “flips” to the outer envelope of the cell membrane (allows macrophages to recognize and phagocytose apoptotic bodies
37
Q

what is the term for phagocytosis of apoptotic cells is so efficient that dead cells often disappear within minutes without leaving a trace

A

efferocytosis

38
Q

when does necroptosis happen?

A
  • seems to be linked to physiologic development (calcification) of the growth plate
  • cell death in steatohepatitis, pancreatitis, ischemia-reperfusion injury
  • maybe parkinson’s deases
39
Q

what is hypertrophy

A

increase in the size of cells -> increase in size of the organ

40
Q

what are the causes of hypertrophy?

A

increased functional demand, hormonal stimulation

41
Q

what does hyperplasia mean?

A

increase in the number of cells in an organ

42
Q

what is atrophy?

A

decrease in the number and/or size of cells

43
Q

what are the phases of autophagy?

A
  • initiation
  • nucleation
  • elongation of isolation membrane
44
Q

autophagy leads to creation of a double-membrane-bound vacuole called what?

A

autophagosome

45
Q

what is pathologic calcification?

A

abnormal tissue deposition of calcium salts

46
Q

what are the 2 forms of pathologic calcification?

A

Dystrophic calcification = calcification in dying tissue
Metastatic calcification = calcification in viable tissue

47
Q

Explain Dystrophic calcification

A
  • Localized in areas of necrosis
  • Usually present in atherosclerotic plaques
  • Whatever the site of deposition, the calcium salts appear macroscopically as fine, white granules or clumps, often felt as gritty deposits
  • Final common pathway is the formation of crystalline calcium phosphate
  • Calcium is concentrated in membrane-bound vesicles in cells by a process that is initiated by membrane damage and has several steps:
    1. Calcium ion binds to the phospholipids present in the vesicle membrane
    2. Phosphatases associated with the membrane generate phosphate groups, which bind to the calcium
    3. The cycle of calcium and phosphate binding is repeated, raising the local concentrations and producing a deposit near the membrane
    4. A microcrystal is formed which can then propagate and lead to more calcium deposition
48
Q

Explain metastatic calcification

A
  • Occurs in normal tissues/cells due to diseases that cause increased levels of serum calcium (hypercalcemia)
  • Tends to affect interstitial tissues of the gastric mucosa, kidneys, lungs, pulmonary veins
49
Q

what are the morphologic patterns of necrosis?

A
  1. Coagulative - architecture of dead cells preserved
  2. Liquefactive - dead cells digested
  3. Caseous - “cheese-like” necrosis, usually seen in TB
  4. Fat Necrosis
50
Q

Coagulative necrosis

A
  • Preservation of basic outline of the coagulated cells
    ○ Eosinophilic “cell ghosts” with no nuclei may persist for weeks
  • Affected tissue has a firm (cooked) texture
  • Injury and increasing intracellular acidosis denature structural proteins and enzyme s -> block proteolysis
  • Necrotic cells eventually removed by fragmentation and phagocytosis of cellular debris = inflammation
  • Typical of necrosis in most solid organs, with the exception of the brain
  • Typical of ischemic damage - i.e. myocardial infarct
51
Q

Liquefactive Necrosis

A
  • Characteristic of focal bacteria or fungal infections -> accumulate inflammatory cells -> completely digests dead cells -> liquid viscous mass
    ○ Microbes stimulate the accumulation of leukocytes and the liberation of enzymes from these cells
  • Typical of necrosis within the brain…although usually not due to infectious processes
    ○ In acute inflammation -> creamy yellow material accumulates because of dead white blood cells = pus
  • In some cases, coagulative necrosis may progress to a liquefactive picture over time
52
Q

Caseous Necrosis

A
  • Distinctive form of coagulative necrosis
  • Found in foci of tuberculosis (TB) infection
  • Cheesy white appearance of area of necrosis, found in the centre of the granuloma
    ○ Under the microscope, the necrotic area is a structure-less collection of debris enclosed within a distinctive inflammatory border
    ○ The entire structure is known as a granuloma
  • Tissue architecture completely obliterated, replaced by the granuloma
53
Q

Fat Necrosis

A
  • Not a specific pattern of necrosis, but refers to a focal area of fat destruction
  • Typically occurs as a result of release of activated pancreatic lipases into the pancreas and the peritoneal cavity
    ○ i.e. acute pancreatitis
  • Activated pancreatic enzymes escape from acinar cells and ducts to liquefy fat cell membranes and split the TG esters contained within fat cells
  • Released FA combine with calcium to produce grossly visible chalky white areas

BMS test 2 (11 decks)

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