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CM test 1 from davida > Cell injury > Flashcards

Cell injury Flashcards

1
Q

True or False, a cell can modify its organization and function in response to stress

A

True. this is called adaptation, and will preserve the health of the cell to a certain point. When the cells adaptive capability is exceeded, cell injury develops.

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2
Q

true or false, cell injury is reversible

A

true. up to a certain point it is reversible, but in the case of persistent, severe stress the cell suffers irreversible injury and dies

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3
Q

which lives longer, aerobic or anaerobic cells?

A

anaerobic cells can live much longer than those that need O2

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4
Q

7 causes of cell injury

A
  1. hypoxia (#1)
  2. physical agents
  3. chemical agents and drugs
  4. infectious agents
  5. immunological reactions
  6. genetic defects
  7. nutritional imbalances
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5
Q

causes of cell injury - Hypoxia
definition-1
causes -3

A
  1. def- decreased availability of O2, which leads to a spectrum of changes, including cell injury to death
    causes:
  2. ischemia (obstruction of blood flow) - most common
  3. cardiopulmonary failure- venous drainage is obstructed by vascular disease =>loss of O2 supply to tissues
  4. loss of O2 carrying capacity of the blood as in anemia or CO poisoning
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6
Q

causes of cell injury- Physical Agents (5 examples)

A
  1. mechanical trauma (getting beat up)
  2. extreme heat or cold
  3. sudden changes in atmospheric pressure
  4. ionizing radiation => formation of OH radicals (ie atomic bombs)
  5. electrical energy
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7
Q

causes of cell injury- Chemical agents and drugs
def
parts of cell chemical agents can affect -3
examples -5

A

def- any chemical agent may generate cell adaption, injury or death by acting on vital cell functions such as:
1. membrane permeability
2. osmotic homeostasis, or
3. integrity of different enzymes
examples of chemical agents:
poisons, air pollutants, pesticides, herbicides, and drugs

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8
Q

causes of cell injury- infectious agents (5)

A

sizes from submicroscopic -> macroscopic forms

  1. viruses
  2. rickettsiae
  3. bacteria
  4. fungi
  5. parasites (worst medical problem world wide)
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9
Q

causes of cell injury- immunologic reactions
explanation/ definition (1)
types (3)

A

def- contradictory to main role of immune system which serves in defense against biological agents, immunologic reactions may cause the following cell injury:

  1. anaphylactic reaction to foreign proteins
  2. immune complexes deposition (things join together to fight virus but complex can precipitate out and cause inflammation)
  3. autoimmune reactions
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10
Q

causes of cell injury- genetic defects
explanation/ definition (1)
types (2)

A

def- results in gross defects in protein structure which are responsible for inborn errors of metabolism
eg:
1. congenital malformations
2. chromosomal- insertions, deletions, translocations or point mutations

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11
Q

causes of cell injury - nutritional imbalances (4)

A
  1. protein/calorie deficiencies
  2. vitamin deficiencies (hypovitaminoses)
  3. vitamin excess (hypervitaminoses)
  4. dietary excess
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12
Q

most common cause of cell injury and how it works

A

ischemia is the most common cause of cell injury. Causes injury by reducing cellular O2 supplies. Usually starts as reversible but if it persists => irreversible injury.

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13
Q 
reversible cell injury 
 def -1
 characteristics - 6
A

if stress is removed in time, full cell integrity can be restored. characteristics of acute injury are:

  1. cell swelling- because it cannot maintain homeostasis
  2. mitochondrial swelling
  3. dilation of endoplasmic reticulum
  4. plasma membrane alterations
  5. nuclear alterations
  6. fatty changes- manifested by appearance of lipid vacuoles. occurs in hepatocyte and myocardial cells
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14
Q 
irreversible cell injury
 def -1
 characteristics - 5
A

persistent, sufficient, severe stress leads to irreversible injury and the cell dies. associated with:

  1. extensive damage to cell membrane
  2. vacuolization of mitochondria
  3. swelling of lisosomes
  4. massive Ca2+ influx into cell
  5. release of O2 free radicals
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15
Q 
scientific wordy characteristics of irreversible cell injury 
 whats happening with enzymes (3) 
 nuclear changes (3)
A 
1. the main characteristic of lethally injured cells is progressive degradation of enzymes followed by enzymic digestion of cell and denaturation of proteins.
nuclear changes that also occur:
2. pyknosis (nuclear shrinkage)
3. karyorrhexis (nucleus fragmentation)
4. karyolysis (nucleus degradation)
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16
Q

three potential causes for cell membrane damage

A
  1. progressive loss of membrane phospholipids- due to activation of endogenous phospholipases by increased cytostolic Ca2+
  2. cytoskeletal abnormalities - increase of intracellular Ca2+ enzymes => detachment of cell membrane from cytoskeleton => membrane susceptible to stretching and rupture
  3. toxic O2 radicals - these are increased in ischemic tissues especially after restoration of blood flow, may be the cause of reperfusion injury.
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17
Q

what is the central factor in irreversible injury?

A

cell membrane damage

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18
Q

2 types of cellular morphological changes

A
  1. acute cell injury (which can be reversible and irreversible)
  2. intracellular accumulations
19
Q

4 patterns of necrosis, after cell death

A
  1. coagulative necrosis
  2. liquefactive necrosis
  3. caseous necrosis
  4. gangrenous necrosis
20
Q

coagulative necrosis (3)
characteristic of…
what happens
what happens to cell outlines

A
  1. characteristic of hypoxic death in cell in all tissues **EXCLUDING THE BRAIN
  2. increased intracellular acidosis denatures proteins and blocks proteolysis of the cell itself
  3. outlines are preserved for a few days but then removed by phagocytosis
21
Q

liquefactive necrosis
characteristic of…
what happens to cell outlines

A
  1. characteristic of BACTERIAL infections and hypoxic (stroke) DEATH OF BRAIN CELLS
  2. results from hydrolytic enzymes including cell autolysis and heterolysis followed by complete dissolution of cell (including outlines)
22
Q

caseous necrosis
what it is
histology

A
  1. combo of coagulative and liquefactive that refers to lesions on TUBERCULOSIS
  2. histologically appears like white and cheese (casein) amorphous debris composed of coagulated cells enclosed w/i inflammatory border called granulomatous reaction
23
Q

gangrenous necrosis
where it happens (and why)
how it starts -> ends
2 types

A
  1. usually lower limb that lost blood supply
  2. starts as coagulative necrosis that became infected and therefore altered by liquefactive action of bacteria and leukocyte enzymes
  3. can by ‘dry’ (coagulative necrosis dominates) or ‘wet’ (liquefactive necrosis dominates)
24
Q

programmed cell death
def -1
scientific wordy explanation -1
physiological and pathological examples -2

A
  1. apoptosis- genetically programmed cell death or destruction
  2. Ca dependent activation of endogenous endonuclease which => fragmentation of DNA and cell changes
  3. physiological example- destruction of cells during embryogenesis and endometrium during menstual cycle
  4. pathological example- irridation or viral infections like hepatitis
25
Q

intracellular accumulations (3)
what they are
what they are a result of
do these occur in normal circumstances?

A
  1. type of morphological change in cell
  2. result of escalated production of endogenous or deposition of exogenous substances and/or inadequate metabolic rate or inability to eliminate accumulating substance
  3. under normal circumstances accumulations may be in cytoplasm or nucleus and are harmless
26
Q

5 types of intracellular accumulations

A
  1. lipid accumulation
  2. protein accumulation
  3. glycogen accumulation
  4. complex lipids and carbohydrate accumulation
  5. pigment accumulation
27
Q 
lipid accumulation (2 types)
 and where it usually occurs
A

type of intracellular accumulation (morphological change)

  1. fatty change: usually occurs in liver, but may also occur in heart (tiger effect), muslces, kidneys, and other organs
  2. macrophage lipid overload (foam cells)
28
Q

glycogen accumulations (3)

A

type of intracellular accumulation (morphological change)

  1. long chain polymers of glucose formed and stored in liver (and to a lesser extend muscles) that increasingly accumulate due to:
  2. abnormalities in glucose metabolism
  3. generic deviation in glycogen metabolism
29
Q 
complex lipid and carbohydrate accumulation (2)
 def and 2 diseases it can lead to
A

type of intracellular accumulation (morphological change)

  1. result of inborn errors in carbs and lipid structures so they cannot be metabolized in the usual fashion
  2. collected in reticulo-endothelial system which results in hepatomegaly and splenomegaly
30
Q 
pigment accumulations 
5 exogenous
 anthracosis
 siderosis
 silicosis
 asbestosis
 tattooing
3 endogenous
 lipofuscian
 melanin
 hemosiderin
A 
exogenous
1. anthracosis- inhalation of coal dust
2. siderosis- inhalation of iron dust
3. silicosis- inhalation of silicone
4. asbestosis- inhalation of asbestos fibers
5. tattooing
endogenous
1. lipofuscian- "aging pigment" yellow-brown pigment in hepatocytes which accumulate over time in liver and heart cells as a result of aging or severe malnutrition
2. melanin- "black pigment"
3. hemosiderin- accumulation of iron
31
Q

gauchers disease
what it is
how it can be diagnosed in childhood

A
  1. inborn errors of glyco-sphingolyoid metabolism

2. hepato-splenomegaly may be noted in childhood

32
Q 
hemosiderin (6)
 basics (2)
 color changes associated with it
 what hemosiderin overload is associated with
 when is usually happens
 what happens if it spreads
A
  1. iron is normally stored in association with a protein apoferritin in a complex called ferritin micelle, hemosiderin is ferritin micelle aggregates
  2. in a common bruise isolated hemorrhage is followed by lysis of erythrocytes and released hemoglobin is transformed => hemosiderin
  3. changes in color- blue-green = biliverdin => green -yellow = biliruben
  4. hemosiderin overload is associated with increased absorption / impaired utilization of iron.
  5. occus in hemolytic anemias and blood transfusions.
  6. may spread to many organs and in extreme cases = hemochromatosis and is associated with damage of liver and pancrease
33
Q

cellular adaptations to injury
def-1
physiological vs pathological adaptation
5 types of cellular adaptations

A
  1. cellular adaptation is a state that lies btwn normal, unstressed cell and injured overstressed cell. in response to persistenet cell cell adapts or dies
  2. physiological adaptations = response to normal stimulation
  3. pathological adaptations = same underylying mechanism but provide cells with ability to modulate environment and escape injury
    5 types of cellular adaptations:
  4. atrophy
  5. hypertrophy
  6. hyperplasia
  7. metaplasia
  8. dysplasia
34
Q

atrophy
def-1
5 reasons for atrophy

A 
atrophy is a type of cellular adaptation to injury.
def- shrinkage of tissue or organ due to loss of cells structural components **not losing #s of cells, cells just getting smaller**
5 reasons for atrophy
1. decreased work load
2. loss of innervation
3. diminished blood supply
4. inadeuate nutrition
5. ageing
35
Q

hypertrophy
def- 1
cause-1
physiologic and pathologic examples

A

hypertrophy is a type of cellular adaptation to injury

  1. def- increase in size of tissue or organ that usually happens due to increased synthesis of structural components **not increasing # of cells, cells getting bigger* (so not cells with miotic division)
  2. can be caused by increased functional demand of tissue or specific hormonal stimulation

conditions it occurs under

  1. physiological- estrogen stimulated growth of uterus during pregnancy
  2. pathological- hypertrophy of striated heart muscle cells induced by increased workload due to interference with aortic outflow or systemic hypertension
36
Q 
heart hypertrophy
 what its caused by
 how heart and skeletal cells adapt 
 what can exercise induced hypertrophy lead to?
 final result of heart hypertrophy
A
  1. caused by increased functional demand due to mechanical interference with aortic outflow or because of systemic hypertension. this requires heart to eject blood under higher pressure
  2. heart and skeletal muscle cells cannot adapt to increased metabolic demands by increased miotic division. to achieve a balance synthesis of more proteins and filaments occur, keeping metabolic activity the same.
  3. exercise induced hypertrophy can lead to heart doubling in weight.
  4. this can all lead to cardiac failure
37
Q

hyperplasia
def -1
physiologic and pathologic examples

A

hyperplasia is a cellular adaptation to injury

  1. def- increase in # of cells in tissue or organ, usually in association with hypertrophy
  2. physiologic cell proliferation- hormonal and compensatory
  3. pathologic cell proliferation- excessive hormonal, chemical or mechanical stimulation
38
Q

metaplasia
def- 1
2 examples

A

metaplasia is a cellular adaptation to injury

  1. def- process of adaptive substitution for cells more sensitive to stress by other types better able to withstand hostile conditions
  2. eg- characteristic of epithelical cells, but may occur in mesenchymal cells
39
Q

dysplasia
def- 1
2 locations usually occurs

A

dysplasia is a cellular adaptation to injury

  1. def- alteration to size, shape and organization in epithelial and mesenchymal cells
  2. usually happens in cervix and respiratory tract- strongly implicated as precursor to cancer at these locations
40
Q

What is tiger effect?

A

fatty accumulation (morphological adaptation) in the heart

41
Q

hepatosplenomegaly is associated with what disease?

A

Gaucher’s disease

42
Q

what is pyknosis?

what is it characteristic of?

A
  1. nuclear shrinkage

2. characteristic of irreversible cell injury

43
Q

what is karyorrhexis?

what is it characteristic of?

A
  1. nucleus fragmentation

2. characteristic of irreversible cell injury

44
Q

what is karyolysis?

what is it characteristic of?

A
  1. nucleus degradation

2. characteristic of irreversible cell injury

CM test 1 from davida (6 decks)

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