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Pathology > cell injury and adaptation > Flashcards

cell injury and adaptation Flashcards

1
Q

Stages in the Cellular Response to Stress and Injury diagram

A
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2
Q

HYPERTROPHY

Pure hypertrophy occurs where?

A

• Hypertrophy –increase in the size of an organ without an increase in cell number
(hyperplasia)
• Pure hypertrophy usually occurs only in skeletal and cardiac muscle

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3
Q

cardiac hypertrophy

A

due to hypertension, done to increase force of contraction

increased size can lead to ischemia resulting in MI/ cell death

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4
Q

HYPERPLASIA

types?

A

Hyperplasia is the increase in size of a tissue or organ due to an increased number of cells
can be physiologic, pathologic or combined with hypertrophy

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5
Q

physiologic hyperplasia examples

A

– Erythroid bone marrow hyperplasia at high altitude
– Cyclic enlargement of the endometrium and breast during the menstrual cycle
– Regrowth of liver parenchyma after surgical excision is compensatory

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6
Q

pathologic hyperplasia example

A

epithelial hyperplasia caused by the human papilloma virus

HPV

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7
Q

combo hypertrophy and plasia examples

A

– In an enlarged uterus of pregnancy, myometrial smooth muscle cells are increased not only in number (hyperplasia) but also in size (hypertrophy)
– In benign prostatic enlargement, there is both hyperplasia and hypertrophy of prostatic glands and smooth muscle

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8
Q

(Squamous) Papilloma

A

epithelial hyperplasia caused by HPV on lips

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9
Q

pyogenic granuloma

A

epithelial hyperplasia presenting as an ulcerative nodule on gingiva

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10
Q

fibroma

A

sessile nodule on the tongue, represents a fibrous hyperplasia

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11
Q

epulis fissuratum

A

represents a fibrous hyperplasia, found with ill-fitting dentures

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12
Q

inflammatory papillary hyperplasia of the palate

A

represents a combo epithelial and fibrous hyperplasia

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13
Q

sub-pontic osseous hyperplasia

A

osseous hyperplasia, bone forms under pontic

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14
Q

exotoses

A

represent osseous hyperplasia

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15
Q

gingival enlargement, common causes?

A

form of hyperplasia often due to poor hygiene or diabetes

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16
Q

drug induced gingival enlargement

A

side effect of some drugs
procardia- ca channel block for hypertension
cyclosporin- immunosuppressant for transplants
dialntin/phentoin- anti-seizure med

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17
Q

possible causes of gingival enlargement

A
  • Inflammatory hyperplasia
  • Drug-induced enlargement
  • Leukemia infiltrates
  • Amyloid infiltration
  • Klippel-Trenaunay-Weber syndrome
  • Juvenile hyaline fibromatosis
  • Cowden syndrome
  • Wegener granulomatosis
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18
Q

condylar hyperplasia

A

Idiopathic unilateral growth of the mandibular condyle

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19
Q

hyperplastic dental follicle

A

enlarged follicle of non erupted tooth, would req a biopsy to diagnose

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20
Q

gynecomastia

A

hyperplasia of the male breast, due to increased estrogen or increased hormone secreting tumor

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21
Q

ATROPHY

A

• Atrophy is the reduction in size of cells, tissues or organs

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22
Q

types of atrophy

A

pathologic and physiological

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23
Q

PATHOLOGIC ATROPHY examples

A
  • Atrophy of skeletal muscle following denervation

* Atrophy of the brain due to ischemia

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24
Q

PHYSIOLOGIC ATROPHY examples

A
  • Atrophy of the uterus after pregnancy

* Involution of the thymus in early adult life

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25
Q

PATHOLOGIC ATROPHY MAY RESULT FROM:

A 
Disuse
• Denervation
• Lack of trophic hormones
• Ischemia - reduction in blood supply
• Malnutrition
• Idiopathic –Parry-Romberg syndrome
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26
Q

thenar atrophy

A

mm atrophy caused by carapl tunnel= lack of medial nn inn

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27
Q

denervation atrophy in skeletal mm

A

loss of inn results in the decrease in mm cell size

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28
Q

atherosclerotic disease of the brain

A

will cause atrophy of the brian = widened gyri and narrow sulci

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29
Q

edentulous atrophy

A

loss of alveolar bone without teeth

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30
Q

PARRY ROMBERG SYNDROME

A

idiopathic PROGRESSIVE HEMIFACIAL ATROPHY= will stabilize and can be corrected with surgery

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31
Q

METAPLASIA

A

• Metaplasia is the replacement of one mature cell type by another one.
• It generally represents a change to a “tougher” cell type
Metaplasia is generally reversible and the tissue reverts to its normal state after the irritant is removed
• If the irritant persists, metaplasia may progress to dysplasia and then to frank neoplasia

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32
Q

smokers metaplasia

A

• Replacement of bronchial stratified columnar epithelium by squamous epithelium is an example of squamous metaplasia that occurs in smokers
can lead to dysplasia and become malignant = squamous cell carcinoma

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33
Q

barrets esophagus

A

• Intestinal metaplasia of the esophagus, called Barrett esophagus is caused by chronic irritation by gastric juices in gastroesophageal reflux
squamous to columnar in the lower esophagus, better able to tolerate acids
can progress to dysplasia and become and adenocarcinoma

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34
Q

NECROTIZING SIALOMETAPLASIA

A

on the palate, a reactive condition that will heal on its own
appearance of epithelial tissue invading surrounding tissue similar to cancer

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35
Q

HOW CELLS RESPOND TO NON-LETHAL INJURY

A

adaptive and non-adaptive

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36
Q

adaptive changes

A

hyperplasia
hypertrophy
metaplasia
atrophy

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37
Q

non adaptive changes

A

mainly developmental or genetic
agenesis
aplasia
hypoplasia

38
Q

agenesis

A

complete non-dev of a cell or organ

examples: mandible, tooth roots, multiple teeth, etc

39
Q

aplasia/hypoplasia

A

• Hypoplasia is the incomplete development of
an organ
• The organ never reached its normal size

40
Q

TREACHER COLLINS SYNDROME

A

MANDIBULO-FACIAL DYSPLASIA, hypoplasia of the mandible

41
Q

Pierre robin syndrome

A

hypoplasia/ aplasia of the mandible

42
Q

regional odotnodysplasia

A

certain quadrants m ay be affected with the hypoplasia/aplasia of teeth
“ghost teeth” present
also represents a dysplasia= abnormal formation

43
Q

DYSPLASIA

A

DYSPLASIA
• Dysplasia literally means abnormal formation
• The term is used in many context

44
Q

What does EPITHELIAL DYSPLASIA potentially lead to? only this?

A

potential to lead to malignancies and cancer

only epithelial dysplasia indicates pre malignancy

45
Q

ECTODERMAL DYSPLASIA

A

genetic/developmental

abnormal formation of ectoderm derivatives (teeth, hair, skin, sweat glands, etc.)

46
Q

FIBRO-OSSEOUS DYSPLASIA at tooth root radiography

A

mixed lucent and opaque radiograph appearance, present at apex

47
Q

fibrous dysplasia of the face

A

usually with maxilla or mandible, become enlarged unilaterally
developmental
seen radiographically

48
Q

type I dentin dysplasia

A

abnormal root dentin formation

49
Q

Stages in the Cellular Response to Stress and Injury diagram

A
50
Q

reversible change in the liver

A

fatty change, due to alcohol abuse, accumulation of fat cells in the liver

51
Q

irreversible changes

A

cell death: apoptosis and necrosis

52
Q

cell death mechanism diagrams

A

apoptosis: apoptotic formed and digested by phagocytes= clean
necrosis: lysosomal membranes break and contents leak digesting cell contents and causing local inflammatory response

53
Q

nuclear signals of necrosis

A
  • Pyknosis –a small, dark and shrunken nucleus
  • Karyorrhexis –nuclear fragmentation
  • Karyolysis –dissolution of the nucleus
54
Q

what tells you how cells die?

A

cytoplasm

55
Q

types of necrosis, usually seen with?

A
  • Coagulative necrosis –typically seen in hypoxic injury (myocardial infarct)
  • Liquefactive necrosis –typically seen in bacterial infections and cerebral infarct
  • Caseous necrosis –necrotic tissue is converted into a cheesy mass (tuberculosis)
  • Fat necrosis –characteristically seen in acute pancreatitis
56
Q
A

coagulative necrosis

57
Q
A

liquefactive necrosis

58
Q
A

causeous necrosis

59
Q

APOPTOSIS

A
  • Programmed cell death occurs through activation of an internal suicide program
  • CASPASES enzymes mediate this
  • Selectively eliminates unwanted cells with minimal disturbance to the surrounding cells
  • The plasma membrane remains intact, but its structure is altered so that the it becomes a target for phagocytosis
  • The dead cell is rapidly cleared before its contents have leaked out and therefore does not elicit an inflammatory reaction
60
Q

types of apoptosis

A

physiologic and pathologic

61
Q

Physiologic apoptosis examples

A
  • Programmed destruction of cells during embryogenesis
  • Hormone-dependent involution of tissues in the adult
  • Deletion of potentially harmful self-reactive lymphocytes
  • Cell death induced by cytotoxic T-cells (virally-infected or neoplastic cells)
62
Q

Pathologic apoptosis examples

A
  • If DNA repair mechanisms can’t cope with damage, the cells kills itself by apoptosis
  • Cell death in certain viral infections (hepatitis)
  • Pathologic atrophy in organs after obstruction
  • Cell death in tumors
63
Q

Exogenous pigments

A

from external environment
– Carbon - anthracosis, blackened lungs
– Tattooing –skin and mucosal tattoos, amalgam tats

64
Q

Endogenous pigments

A

– Lipofuscin (aging)
– Melanin –formed in melanocytes
– Hemosiderin –hemoglobin-derived
– Bilirubin, excreted in bowels/urine

65
Q

PATHOLOGIC CALCIFICATION

A

• Pathologic calcification is the abnormal deposition of calcium salts in tissue, can be dystrophic ot metastic

66
Q

dystrophic calcification

A

• Dystrophic calcification occurs in nonviable or dying tissues in the presence of normal serum calcium levels

67
Q

metastatic calcification

A

Metastatic calcification occurs in viable tissues and is associated with hypercalcemia

68
Q
A

cardiac hypertrophy

69
Q
A

epithelial hyperplasia: papilloma

70
Q
A

ENDOTHELIAL HYPERPLASIA:

Pyogenic Granuloma

71
Q
A

FIBROUS HYPERPLASIA:

Fibroma

72
Q
A

FIBROUS HYPERPLASIA:

Epulis Fissuratum

73
Q
A

EPITHELIAL & FIBROUS HYPERPLASIA:

INFLAMMATORY PAPILLARY HYPERPLASIA

74
Q
A

OSSEOUS HYPERPLASIA:

SUB-PONTIC OSSEOUS HYPERPLASIA

75
Q
A

OSSEOUS HYPERPLASIA:

Exostoses

76
Q
A

GINGIVAL ENLARGEMENT (HYPERPLASIA)

77
Q
A

condylar hyperplasia

78
Q
A

hyperplastic dental follicle

79
Q
A

brain atrophy, atherscerlotic disease

80
Q
A

parry romberg syndrome

81
Q
A

barretts esphogus, metaplasia

82
Q
A

NECROTIZING SIALOMETAPLASIA

83
Q
A

mandibular agenesis

84
Q
A

root agenesis

85
Q
A

MANDIBULO-FACIAL DYSPLASIA

TREACHER COLLINS SYNDROME

86
Q
A

APLASIA/HYPOPLASIA

REGIONAL ODONTODYSPLASIA

87
Q
A

epithelial dysplasia

88
Q
A

ectodermal dysplasia

89
Q
A

fibro ossesoius dysplasia

90
Q
A

fibrous dysplasia

91
Q
A

dentin dysplasia type I

92
Q

how are these nuceli identified? what is happening?

A

pyknosis and karyohexis, cell death

Pathology (19 decks)

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