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Foundations of Medicine 1 > Cell Adaption and Injury > Flashcards

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
Q

Glycogen generally accumulates in what kind of patients and what does it look like?

A

May accumulate in patient with abnormalities in glycogen or glucose metabolism (DM II)
Generally appear as clear, cytoplasmic vacuoles in H &E staining

26
Q

Lipofuscin

A

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
Q

Hemosiderin

A

a golden yellow-brown pigment that is the result of blood breakdown with iron

28
Q

Bilirubin

A

a yellow pigment derived from blood breakdown with no iron

29
Q

What are the major causes of cell injury?

A 
Hypoxia
Physical agents
chemical agents/ drugs
infection 
immunologic reactions and derangements
genetic derangements
nutritional deficiencies and imbalances
30
Q

What are the 4 major targets of cell injury?

A

biochemical machinery for aerobic respiration (ATP production)
integrity of cell membranes
protein synthesis
integrity of the genetic apparatus of the cell

31
Q

Depletion of ATP leads to what 5 things?

A

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
Q

What 3 things cause mitochondrial damage?

A

increase in Ca++, ROS, and oxygen deprivation

33
Q

What 3 consequences result as a result of Ca++ influx?

A

1) opening of the mitochondrial permeability transition pore (cyt c)
2) activation of numerous enzymes (ases)
3) direct activation of caspases, inducing apoptosis

34
Q

What are the principal free radicals?

A

OH
O2
H2O2
ONOO

35
Q

What are the 3 main consequences of free radicals in cell injury?

A

1) lipid peroxidation and membrane damage
2) oxidative modification of proteins–> protein damage
3) lesions in DNA

36
Q

What are the 5 sources of free radicals?

A

1) by products of mitochondrial oxidative phosphorylation
2) leukocytes (inflammation)
3) metals (Fe and copper)
4) radiant energy
5) NO

37
Q

What 3 agents remove free radicals?

A

1) antioxidants
2) transfer proteins (transferrin, ferritin, ceruloplasmin)
3) enzymes

38
Q

Describe the 4 major steps to apoptotic cell death?

A

1) cell shrinkage and increased density of cytoplasm
2) Nuclear pyknosis
3) cytoplasmic blebs
4) apoptotic bodies

39
Q

Describe the mophological signs of reversible injury?

A 
EM
1) plasma blebbing and loss  of microvilli
2) mitochondrial swelling
3) dilation of endoplasmic reticulum
LM
1) cellular swelling
2) fatty change
40
Q

Describe the signs of irreversible injury

A 
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
Q

Which necrosis is associated with ischemia?

A

coagulative

42
Q

Which necrosis is associated with bacterial and fungal infections?

A

fungal/bacterial

43
Q

Which type of necrosis is associated with TB?

A

caseous

44
Q

which necrosis is associated with pancreatitis and leakage of pancreatic lipases?

A

fat necrosis

Foundations of Medicine 1 (12 decks)

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