Cell injury: irreversible Flashcards

(41 cards)

1
Q

define cell injury

A

The basis of all diseases is injury to the smallest living unit of the body, cld cell.

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2
Q

causes of cell injury

A
  1. Hypoxia (deficiency of oxygen)
  2. physical agent
  3. biological agents
  4. chemical agents + drugs
  5. Endogenous toxins
  6. Immunologic rx (hypersensitivity)
  7. Nutritional imbalance
  8. Genetic abnormalities
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3
Q

in causes of cell injury: hypoxia is due to

A

(i) Ischaemia
(ii) Decrease of o2 carrying capacity of bld due to anemia, cardiac or respiratory failure and CO poisoning.

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4
Q

in causes of cell injury: physical agent eg

A
  • burns
  • deep cold
  • radiation
  • mechanical trauma
  • electric shock
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5
Q

in causes of of cell injury: biological agents eg

A

viruses
bacterial toxins
fungi
parasites.

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6
Q

in causes of cell injury: chemical agent and drugs eg

A

alkalis
acids
insecticides
alcohol
narcotic drugs
air pollutants

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7
Q

in causes of cell injury: Endogenous toxins eg

A

uremia
jaundice
diabetic ketosis

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8
Q

in causes of cell injury: Nutritional imbalance eg

A

protein calorie malnutrition
starvation
obesity
diabetes mellitus
deficiency of other substances and vitamins.

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9
Q

what r the pathogenesis Of Cell Injury?
Hypoxic and ischemic injury to the cells occur through:

A

(A)- ATP depletion
(B)- over production of o2 – derived free radicals due to imbalance
b2iann free radicals generation + radical defense system.
(C)-Defect in membrane selective permeability
(D)- Increased intracellular ca+ and loss of ca+ homeostasis that result from damage of both cell membrane & mitochondrial membrane and ER.

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10
Q

what does the increased intracellular Ca+ cause?

A

activation of degenerative cellular enzymes as:
protease
ATPase
phospholipase
endonuclease. (that cause damage & mutation of the nucleus)

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11
Q

Irreversible Cell Injury…

A

Severe stimuli leads to necrosis & apoptosis

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12
Q

Reversible Cell Injury…

A

Mild stress for short duration leads to biochemical change
or
mild form of morphologic change in the affected cells (hydropic swelling).

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13
Q

what is the def of necrosis?

A
  • is local death of cells
  • while the individual is alive
  • followed by morphological changes - in the surrounding living tissue.
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14
Q

what r the causes of cell necrosis?

A

viruses
ischaemia
bacterial toxins
hypersensitivity
ionizing radiation.

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15
Q

when does the Morphologic Change In Necrosis appear?

A

The changes don’t appear in the affected cells by light microscopy before 2-6 hours according to
the type of the affected tissue.

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16
Q

what r the changes in cytoplasm that. take place in necrosis?

A
  1. Swelling + granularity of cytoplasm.
  2. Loss of cellular membrane.
  3. Fusion of cells.
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17
Q

what r the Nuclear changes that happen in necrosis?

A

I.Pyknosis eg n becomes shrunken condensed and deeply stained.
II.Karyorrhexis: rupture of nuclear membrane w/ fragmentation of n.
III. Karyolysis: n dissolves + disappears.

18
Q

what happens to the effected tissue in necrosis?

A

the affected tissue changes to homogeneous eosinophilic mass with nuclear debris

19
Q

What Is The Morphologic Pattern Of Necrotic Cell Mass?

A
  1. Coagulative necrosis special types of necrosis.
  2. Liquefactive necrosis.
  3. Caseous necrosis.
  4. Fat necrosis.
  5. Gangrenous Necrosis.
  6. Fibrinoid necrosis.
  7. Zinker’s Necrosis .
20
Q

all available info on Coagulative necrosis:

A

It is caused by sudden ischaemia e.g. infarction of heart, kidney + spleen.

Grossly :
- It appears dry pale opaque.
- It is TRIANGULAR: due to the fan like distribution of the supplying bv.
- The infarct area is surrounded by narrow zone of inflammation and congestion.

Microscopically:
-The structural outline of the affected tissue is preserved
- but the cellular details are lost

21
Q

talk about Liquifactive Necrosis:

A
  • The necrosed tissue undergoes rapid softening
    e.g.
    1)infarction of nervous tissue (brain)
    2) suppurative inflammation (Abscess)

 Grossly: the affected tissue appears as homogenous amorphous substance.

 Microscopically: it appears as homogenous eosinophilic structure.

22
Q

what is zat Caseous Necrosis

A

***it is characteristic of tuberculosis.

  • The necrotic tissue undergoes slow partial liquefaction forming yellow cheesy material.

Microscopically:
. It shows amorphous granular eosinophilic material
. lacking the cell outlines.

Grossly
. the caseous material resembles clumpy cheese (caseous necrosis)

23
Q

what is the cause of necrosis in TB?

A

Is the hypersensitivity reaction caused by tuberculoprotein content of the cell wall of Mycobacterium.

24
Q

rant about fat necrosis?!

A

It is necrosis of adipose tissue including two types:
1.Traumatic: caused by trauma to adipose tissue
e.g. breast and subcutaneous tissue. 2. Enzymatic: which occurs in case
of acute haemorrhagic pancreatitis.

25
Gangrenous Necrosis................
* Due to area of coaculative necrosis followed by putrefaction dry gangrene. OR * When the liquifactive action of the bacteria is more pronounced it is cld wet gangrene.
26
not important but who is Fibrinoid Necrosis?
(A) Collagen diseases (eg. Rheumatic fever, Rheumatoid, Sclerodermia, Lupus erythematosus and Polyarteritis nodosa). (B) In the wall of bv in malignant hypertension
27
also not important but what is Zenker’s Necrosis
Of the rectus abdominus muscle and diaphragm as a complication of : -Bacterial infection particularly typhoid fever. -The striated muscles lose its striation, swell and fuse together in homogeneous structureless mass.
28
what r the Fates And Local Effects Of Necrosis :
1. A small area undergoes repair: forms inflammation 2. If the necrotic area is wide: granulation then gliosis 3. Old unabsorbed caseous: becomes heavily calcified (dystrophic calcification) 4-when the necrotic tissue is infected with putrefactive Organism-=Gangrene
29
what r za General Effects Of Necrosis?
1. Release of enzymes from the breakdown tissue into the bld forms the basis of clinical tests for diagnosis e.g. detection of transamenase in myocardial infarction and liver necrosis in hepatitis. 2. Absorption of dead products into the circulation leads to leukocytosis and fever (Not diagnostic)
30
define apoptosis?
It is programmed death of cells in living tissues.
31
list how apoptosis differs from necrosis
 Occurs in both physiological and pathological conditions.  Starts by nuclear changes in the form of chromatin condensation and fragmentation followed by cytoplasmic budding and then phagocytosis of the extruded apoptotic bodies.  Plasma membrane are thought to remain intact during apoptosis until the last stage so does not initiate inflammatory reaction around it.
32
MAJOR CRITERIA OF APOPTOSIS:
1- Morphological changes 2- Chromatin condensation 3- DNA fragmentation 4- Cell death
33
what r Examples of physiologic and pathologic cases accompanied with apoptosis???
1. Programmed cell death during embryogenesis. 2. Hormone dependent cell involution in case of endometrial cell break down during menstrual cycle. 3. Cell death in tumours during regression induced by cytotoxic drugs or irradiation. 4.In some viral disease e.g. viral hepatitis in which apoptotic cells are known as councilman bodies.
34
what is the stimuli/ etiology of necrosis?
Hypoxia and Toxins
35
what is the stimuli/ etiology for apoptosis?
Physiologca an Pathological
36
what is the Histologic Appearance of necrosis??
Cellular swelling/ burst Releasing their intracellular contents and nuclear changes (pyknosis, Karyohexsis & karyolysis)
37
what is the histological appearance of apoptosis??
Single cell death cells shrink choramatin condensation apoptotic bodies which r engulfed by surrounding cells
38
what happens to the cell size in necrosis??
enlarged
39
what happens to the cell size in apoptosis??
Reduced (shrinkage)
40
Plasma membrane in necrosis is _____ and in apoptosis_______
Disrupted Intact
41
Adjacent inflammation in necrosis is _____ and in apoptosis_______
Present Absent