Cell Injury, Cell Death, and Adaptations

1
Cell Injury, Cell Death, and Adaptations
2
Cell adaptation

• Hypertrophy
• Hyperplasia
• Atrophy
• Metaplasia

3
Hypertrophy Vs. Hyperplasia
4

• B, Small spindle-shaped uterine smooth muscle
  cells from a normal uterus. Compare this with (C)
  large, plump hypertrophied smooth muscle cells
  from a gravid uterus.

5
Physiologic hypertrophy of the uterus during
pregnancy. A, Gross appearance of a normal uterus
(right) and a gravid uterus (left)
6

• This is cardiac hypertrophy involving the left
  ventricle. The number of myocardial fibers does
  not increase, but their size can increase in
  response to an increased workload, leading to the
  marked thickening of the left ventricle in this
  patient with systemic hypertension.

7

• Here is one of the nodules of hyperplastic
  prostate, with many glands along with some
  intervening stroma. The cells making up the
  glands are normal in appearance, but there are
  just too many of them.

8

• Nodular Prostatic Hyperplasia

9

• The prominent folds of endometrium in this uterus
  opened to reveal the endometrial cavity are an
  example of hyperplasia. Cells forming both the
  endometrial glands and the stroma have increased
  in number. As a result, the size of the
  endometrium has increased. This increase is
  physiologic with a normal menstrual cycle.

10
Atrophy
11

• The testis at the right has undergone atrophy and
  is much smaller than the normal testis at the
  left.

12

• This is cerebral atrophy in a patient with
  Alzheimer disease. The gyri are narrowed and the
  intervening sulci widened.

13
(No Transcript)
14
Metaplasia
15

• Metaplasia of normal columnar (left) to squamous
  epithelium (right) in a bronchus, shown (A)
  schematically and (B) histologically.

16

• Metaplasia of laryngeal respiratory epithelium
  has occurred here in a smoker. The chronic
  irritation has led to an exchanging of one type
  of epithelium (the normal respiratory epithelium
  at the right) for another (the more resilient
  squamous epithelium at the left).

17

• Metaplasia of the normal esophageal squamous
  mucosa has occurred here, with the appearance of
  gastric type columnar mucosa.

18
Cell Death
19
Necrosis Vs. Apoptosis
20

• This microscopic appearance of myocardium is a
  mess because so many cells have died that the
  tissue is not recognizable. Many nuclei have
  become pyknotic (shrunken and dark) and have then
  undergone karorrhexis (fragmentation) and
  karyolysis (dissolution). The cytoplasm and cell
  borders are not recognizable.

21

• Here is myocardium in which the cells are dying.
  The nuclei of the myocardial fibers are being
  lost. The cytoplasm is losing its structure,
  because no well-defined cross-striations are
  seen.

22

• In this example, liver cells are dying
  individually (arrows) from injury by viral
  hepatitis. The cells are pink and without nuclei.

23

• In this fetal thymus there is involution of
  thymic lymphocytes by the mechanism of apoptosis.
  Individual cells fragment and are consumed by
  phagocytes to give the appearance of clear spaces
  filled with cellular debris.

24
Patterns of Tissue Necrosis
25
Coagulative Necrosis
26

• Two large infarctions (areas of coagulative
  necrosis) are seen in this sectioned spleen.
  Since the etiology of coagulative necrosis is
  usually vascular with loss of blood supply, the
  infarct occurs in a vascular distribution. Thus,
  infarcts are often wedge-shaped with a base on
  the organ capsule.

27

• This is an example of coagulative necrosis. This
  is the typical pattern with ischemia and
  infarction (loss of blood supply and resultant
  tissue anoxia). Here, there is a wedge-shaped
  pale area of coagulative necrosis (infarction) in
  the renal cortex of the kidney.

28

• Microscopically, the renal cortex has undergone
  anoxic injury at the left so that the cells
  appear pale and ghost-like. There is a
  hemorrhagic zone in the middle where the cells
  are dying or have not quite died, and then normal
  renal parenchyma at the far right. This is an
  example of coagulative necrosis.

29

• The contrast between normal adrenal cortex and
  the small pale infarct is good. The area just
  under the capsule is spared because of blood
  supply from capsular arterial branches. It
  illustrates the shape and appearance of an
  ischemic (pale) infarct well.

30
Liquefactive Necrosis
31

• The liver shows a small abscess here filled with
  many neutrophils. This abscess is an example of
  localized liquefactive necrosis.

32

• This is liquefactive necrosis in the brain in a
  patient who suffered a "stroke" with focal loss
  of blood supply to a portion of cerebrum. This
  type of infarction is marked by loss of neurons
  and neuroglial cells and the formation of a clear
  space at the center left.

33

• At high magnification, liquefactive necrosis of
  the brain demonstrates many macrophages at the
  right which are cleaning up the necrotic cellular
  debris.

34

• Grossly, the cerebral infarction at the upper
  left here demonstrates liquefactive necrosis.
  Eventually, the removal of the dead tissue leaves
  behind a cavity.

35
Fat Necrosis
36

• This is fat necrosis of the pancreas. Appear
  grossly as the soft, chalky white areas seen here
  on the cut surfaces.

37
(No Transcript)
38

• Microscopically, fat necrosis adjacent to
  pancreas is seen here. There are some remaining
  steatocytes at the left which are not necrotic.
  The necrotic fat cells at the right have vague
  cellular outlines, have lost their peripheral
  nuclei, and their cytoplasm has become a pink
  amorphous mass of necrotic material.

39
Caseous Necrosis
40

• This is the gross appearance of caseous necrosis
  in a hilar lymph node infected with tuberculosis.
  The node has a cheesy tan to white appearance.

41

• This is more extensive caseous necrosis, with
  confluent cheesy tan granulomas in the upper
  portion of this lung in a patient with
  tuberculosis.

42

• Microscopically, caseous necrosis is
  characterized by acellular areas, as the tissue
  architecture is completely lost (at the upper
  right), surrounded by a granulomatous
  inflammatory process.

43
Gangrenous Necrosis
44

• This is gangrene of the lower extremity. In this
  case the term "wet" gangrene is more applicable
  because of the liquefactive component from
  superimposed infection in addition to the
  coagulative necrosis from loss of blood supply.
  This patient had diabetes mellitus.

45

• Gangrenous necrosis involves the tissues of a
  body part. The inflammation seen here is
  extending beneath the skin of a toe to involve
  soft tissue (fat and connective tissue) and bone.

46
Intracellular Accumulations
47

• Here is fatty change of the liver due to
  accumulation of lipid in the cytoplasm of
  hepatocytes.

48

• Here are Mallory bodies (the red globular
  material) composed of cytoskeletal filaments in
  liver cells chronically damaged from alcoholism.
  These are a type of "intermediate" filament
  between the size of actin (thin) and myosin
  (thick). (proteins accumulation)

49

• Here are neurofibrillary tangles in neurons of a
  patient with Alzheimer's disease. The
  cytoskeletal filaments are grouped together in
  the elongated tangles.

50

• The yellow-brown granular pigment seen in the
  hepatocytes here is (lipofuscin) which
  accumulates over time in cells (particularly
  liver and heart) as a result of "wear and tear"
  with aging.

51

• The brown coarsely granular material in
  macrophages in this alveolus is hemosiderin that
  has accumulated as a result of the breakdown of
  RBC's and release of the iron in heme. The
  macrophages clear up this debris, which is
  eventually recycled.

52

• Here is anthracotic pigment in macrophages in a
  hilar lymph node. Anthracosis is nothing more
  than accumulation of carbon pigment from
  breathing dirty air. Smokers have the most
  pronounced anthracosis.

53

• The black streaks seen between lobules of lung
  beneath the pleural surface are due to
  accumulation of anthracotic pigment. This
  anthracosis of the lung is not harmful and comes
  from the carbonaceous material breathed in from
  dirty air typical of industrialized regions of
  the planet. Persons who smoke would have even
  more of this pigment.

54
Pathologic Calcification
55

• This is dystrophic calcification in the wall of
  the stomach. At the far left is an artery with
  calcification in its wall. There are also
  irregular bluish-purple deposits of calcium in
  the submucosa.

56

• Calcification of the aortic valve. A view looking
  down onto the unopened aortic valve in a heart
  with calcific aortic stenosis. The semilunar
  cusps are thickened and fibrotic. Behind each
  cusp are large, irregular masses of dystrophic
  calcification that will prevent normal opening of
  the cusps.

57

• Here is so-called "metastatic calcification" in
  the lung of a patient with a very high serum
  calcium level (hypercalcemia).

58

• THANK YOU