02/16a Cell Injury I - Adaptation, Injury, and Necrosis Flashcards Preview

Exam 1 > 02/16a Cell Injury I - Adaptation, Injury, and Necrosis > Flashcards

Flashcards in 02/16a Cell Injury I - Adaptation, Injury, and Necrosis Deck (26)
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1
Q

What is the cellular adaption to increased metabolic demand?

A

Hyperplasia or hypertrophy

2
Q

What is the cellular adaptation to decreased stimulation or nutrients?

A

Atrophy

3
Q

What is the cellular adaptation to chronic irritation

A

Metaplasia

4
Q

What is a cellular adaption? When does it happen?

A

Reversible change that occurs in response to stress

5
Q

What happens to a cell if it become irreversibly injured?

A

Undergoes necrosis or apoptosis

6
Q

What is hypertrophy?

A

Increase in the SIZE of cells which results in increased size of the organ
Can be physiological or pathological

7
Q

What are two examples of physiologic hypertrophy?

A

Increased workload on skeletal and cardiac muscle in athletes
Hormone induction in the pregnant uterus

8
Q

What is hyperplasia?

A

Increase in the NUMBER of cells which results in increased size of the organ
Can be physiological or pathological

9
Q

What are two causes of physiological hyperplasia, with examples?

A

Hormonal - female breast during puberty and pregnancy

Compensatory - renal hyperplasia after unilateral nephrectomy, erythroid hyperplasia of bone marrow in mountain climbers

10
Q

What are two causes of pathological hyperplasia, with examples?

A

Excessive hormone stimulation - endometrial hyperplasia during menopause, prostatic hyperplasia
Viral infections - papilloma virus warts on the skin

11
Q

What is atrophy?

A

Reduction in size of an organ due to a decrease in cell size AND number

12
Q

What are seven causes of atrophy? Give examples of each

A

Decreased workload (disuse) - limbs that have been immobilized in casts
Loss of innervation (denervation) - loss of muscle tone in patients with spinal injuries and paralysis
Diminished blood supply (ischemia) - smaller legs in patients with severe peripheral atherosclerosis
Inadequate nutrition - marasmus (inadequate protein), cachexia (cancer)
Loss of endocrine stimulation - uterus and ovaries after menopause
Aging - old people shrink!
Pressure - enlarging benign tumor encroaching on surrounding structures

13
Q

What are four mechanisms of atrophy?

A

1) Decreased protein synthesis
2) Increased protein degradation
3) Ubiquitin-proteasome pathway - degrades proteins
4) Autophagic vacuoles with lipofuscin granules

14
Q

What is metaplasia? When does it occur?

A

Reversible change in which one differentiated cell type is replaced by another cell type
Usually occurs in response to stress or chronic irritation

15
Q

What are three causes and examples of metaplasia?

A

Tobacco smoke –> squamous metaplasia in the respiratory tract
Gastric acid reflux –> gastric metaplasia of the distal esophagus, which can lead to Barrett’s esophagus and cancer
Repeated skeletal muscle injury with hemorrhage –> muscle replaced by bone (myositis ossificans), quite rare

16
Q

What are three possible mechanisms of metaplasia?

A

1) Re-programming of stem cells that exist in normal tissue
2) Induction by cytokines, growth factors, or other environmental signals
3) Retinoic acid

17
Q

What are the two BROAD types of cell injury and death?

A

Reversible

Irreversible (necrosis and apoptosis)

18
Q

What are seven causes of cell injury?

A
Oxygen deprivation (hypoxia or ischemia)
Physical agents (trauma)
Chemical agents and drugs
Infectious agents
Immunologic reactions
Genetic derangements
Nutritional imbalances
19
Q

What are the two major morphologic alterations involved in reversible cell injury?

A

Cellular swelling

Fatty change

20
Q

What are the cytoplasmic and nuclear morphologic alterations involved in irreversible cell injury?

A

Cytoplasmic eosinophilia
Karyolysis - nucleus becomes pale and disappears
Pyknosis - chromatin condenses, nucleus shrinks and becomes deeply basophilic
Karyorrhexis - nucleus undergoes fragmentation

21
Q

What are the five patterns of tissue necrosis?

A
Coagulative 
Liquefactive
Fat necrosis
Caseous
Fibrinoid
22
Q

What are the major characteristics of coagulative necrosis?

A

Progressive loss of cell structure
Coagulation of cellular constituents
Persistence of cellular outlines, until inflammatory cells arrive and degrade them
Changes in cytoplasmic staining (eosinophilia)
Changes in nuclear morphology (pyknosis, karyolysis, karyorrhexis)

23
Q

What are the major characteristics of liquefactive necrosis?

A

Dissolution of necrotic cells
Typically seen in an abscess - large numbers of neutrophils release hydrolytic enzymes that break down the dead cells and form pus
Common in the CNS

24
Q

What are the major characteristics of caseous necrosis?

A

Occurs with granulomatous inflammation in response to certain microorganisms (TB)
Chronic inflammatory response - “cheesy” area of cellular debris in the center of a caseating granuloma

25
Q

What are the major characteristics of fat necrosis?

A

Formation of insoluble salts from the binding and precipitation of free fatty acids (mobilized from adipose tissue by lipases) with calcium ions
Appear chalky white upon gross examination
Basophilic after H&E stain

26
Q

What are the major characteristics of fibroid necrosis?

A
Occurs in the wall of arteries in cases of vasculitis
Necrosis of smooth muscle cells in the tunica media and endothelial damage
Plasma proteins (fibrin) are depositing in the area of necrosis