Cell Adaption and Injury Flashcards

1
Q

Hyperplasia

A

Increase in the number of cells in an organ/tissue

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2
Q

Hypertrophy

A

An increase in the size of individual cells

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3
Q

Atophy

A

decrease in cell size

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4
Q

Metaplasia

A

One adult cell type is replaced by another adult cell type

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5
Q

Hyaline Change

A

This is a descriptive term→ a glassy, pink appearance seen in H&E staining

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6
Q

necrosis

A

form of cell death that is associated with damage from an external source that overwhelms the cell’s ability to survive

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7
Q

anthracosis

A

inhaled and phagocytosed by macrophages in the alveoli; black

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8
Q

caspase

A

are a family of protease enzymes playing essential roles in programmed cell death and inflammation

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9
Q

nuclear pyknosis

A

small,dark chromatin. Due to chromtin condensation and cleavage.

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10
Q

Coagulative necrosis

A

dead tissue is preserved for a few days

Associated with ischemia

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11
Q

liquefactive necrosis

A

dead cells are completely digested, leaving only viscous liquid; Associated with bacterial and fungal infections and hypoxic tissue

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12
Q

Caseous necrosis

A

“cheesy” granular material

Associated with tuberculous infection

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13
Q

Fat necrosis

A

areas of fat destruction in which fatty acids products combine with calcium to produce chalky-white areas;
Associated with pancreatitis and leakage of pancreatic lipase into adjacent tissues

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14
Q

Dystrophic calcification

A

deposition of calcium salts in dying tissue

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15
Q

karyolysis

A

fading of chromatin

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16
Q

karyorrhexis

A

chromatin fragmentation

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17
Q

Metastatic calcification

A

occurs when there is increase serum calcium, and often happens in otherwise normal tissue

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18
Q

Proliferation of glandular breast tissue and endometrial growth occurring as a result of excessive estrogen stimulations are examples of what?

A

hyperplasia

19
Q

muscle growth due to weight lifting and growth of the heart as a result of chronic hypertension is an example of what?

A

hypertrophy

20
Q

Cell Adaption

A

Occurs as a result of chronic stimulation by relatively low level stress

21
Q

Where does steatosis usually occur and what does it look like histologically?

A

Common in liver (alcohol damage)

Appears as round, clear spaces in the cytoplasm

22
Q

What does atherosclerosis look like?

A

internally: cholesterol gives a foamy appearance
Extracellularly: cholesterol molecules tend to crystallize and appear as shard-like

23
Q

Describe amyloidosis

A

Amyloid are small, non-branching fibrils that physically resemble one another
These proteins fold abnormally and are associated with deposition which can lead to pressure atrophy of adjacent cells
Common histologic appearance: hyaline
Stained using Congo Red Stain

24
Q

What causes hyaline change?

A

intracellular or extracellular accumulations of proteins

25
Glycogen generally accumulates in what kind of patients and what does it look like?
May accumulate in patient with abnormalities in glycogen or glucose metabolism (DM II) Generally appear as clear, cytoplasmic vacuoles in H &E staining
26
Lipofuscin
a brown-yellow pigment that results from an incomplete breakdown of old subcellualr components; “wear and tear pigment”; commonly seen in the heart and liver of aging patients
27
Hemosiderin
a golden yellow-brown pigment that is the result of blood breakdown with iron
28
Bilirubin
a yellow pigment derived from blood breakdown with no iron
29
What are the major causes of cell injury?
``` Hypoxia Physical agents chemical agents/ drugs infection immunologic reactions and derangements genetic derangements nutritional deficiencies and imbalances ```
30
What are the 4 major targets of cell injury?
biochemical machinery for aerobic respiration (ATP production) integrity of cell membranes protein synthesis integrity of the genetic apparatus of the cell
31
Depletion of ATP leads to what 5 things?
1) cell swelling ( Na/K pump) 2) decease in pH (LA) 3) abnormal protein folding 4) decrease in protein synthesis 4) increase in Ca++
32
What 3 things cause mitochondrial damage?
increase in Ca++, ROS, and oxygen deprivation
33
What 3 consequences result as a result of Ca++ influx?
1) opening of the mitochondrial permeability transition pore (cyt c) 2) activation of numerous enzymes (ases) 3) direct activation of caspases, inducing apoptosis
34
What are the principal free radicals?
OH O2 H2O2 ONOO
35
What are the 3 main consequences of free radicals in cell injury?
1) lipid peroxidation and membrane damage 2) oxidative modification of proteins--> protein damage 3) lesions in DNA
36
What are the 5 sources of free radicals?
1) by products of mitochondrial oxidative phosphorylation 2) leukocytes (inflammation) 3) metals (Fe and copper) 4) radiant energy 5) NO
37
What 3 agents remove free radicals?
1) antioxidants 2) transfer proteins (transferrin, ferritin, ceruloplasmin) 3) enzymes
38
Describe the 4 major steps to apoptotic cell death?
1) cell shrinkage and increased density of cytoplasm 2) Nuclear pyknosis 3) cytoplasmic blebs 4) apoptotic bodies
39
Describe the mophological signs of reversible injury?
``` EM 1) plasma blebbing and loss of microvilli 2) mitochondrial swelling 3) dilation of endoplasmic reticulum LM 1) cellular swelling 2) fatty change ```
40
Describe the signs of irreversible injury
``` EM 1) membrane discontinuity 2) marked swelling of mitochondria 3) myelin figures LM 1 ) cytoplasmic eosinophilia (dark pink cytoplasm) 2) calcification of fatty acids 3) nuclear changes--> karyolysis, pyknosis, karyorrhexis (chromatin fragmentation) and loss of nucleus ```
41
Which necrosis is associated with ischemia?
coagulative
42
Which necrosis is associated with bacterial and fungal infections?
fungal/bacterial
43
Which type of necrosis is associated with TB?
caseous
44
which necrosis is associated with pancreatitis and leakage of pancreatic lipases?
fat necrosis