Cell Injury I - Ii

Front 1

What characteristics accompany Apoptosis?

Back 1

Cell Shrinkage, Specific DNA Fragmentation, NO INFLAMATION

Front 2

What characteristics accompany Necrosis?

Back 2

Cell Swelling, Random nuclear fragmentation and inflammation.

Front 3

Cell Shrinkage, Specific DNA Fragmentation, NO INFLAMATION are associated with?

Back 3

Apoptosis

Front 4

Cell Swelling, Random nuclear fragmentation and inflammation are associated with?

Back 4

Necrosis

Front 5

Describe Apoptosis

Back 5

A form of cell suicide that is orchestrated by genes. It affects single cells and does not induce an inflammatory response.

Front 6

What enzymes are responsible for protein cleavage during Apoptosis?

Back 6

Caspases - digest nuclear and cytoplasmic proteins and activate endonucleases

Front 7

What activates endonucleases during Apoptosis?

Back 7

Caspases

Front 8

Which gene induces Apoptosis?

Back 8

P53

Front 9

Which gene inhibits Apoptosis?

Back 9

Bcl-2

Front 10

Which protein activates Caspases during Apoptosis?

Back 10

cytochrome-c

Front 11

What is the final phase of Apoptosis?

Back 11

Removal of dead cell fragments by phagocytosis (no inflammatory response)

Front 12

List 5 morphological changes associated with Apoptosis.

Back 12

cell shrinkage, chromatin condensation with peripheral clumping, surface blebs, fragmentation into apoptotic bodies and ingestion by macrophages

Front 13

List 4 examples of Apoptosis.

Back 13

implantation, hepatic cell death in viral infection, lining of uterus during menstruation and deletion of auto-reactive t-cells in the thymus

Front 14

What causes Coagulative necrosis?

Back 14

denaturation of cellular proteins

Front 15

What tissues are affected by Coagulative necrosis?

Back 15

solid organs (ex: heart, intestines, kidney and liver)

Front 16

Name an event that can cause Coagulative necrosis.

Back 16

Myocardial Infarction (associated with ischemia)

Front 17

Name an event that can cause liquifactive necrosis.

Back 17

tissue digestion by phagocytes (hydrolytic enzymes)

Front 18

Infarction causes what type of necrosis in the CNS?

Back 18

liquifactive necrosis - leaves watery cavities in the brain

Front 19

What type of necrosis is Dry Gangrene?

Back 19

Coagulative necrosis occurring over a large area

Front 20

What type of Gangrene involves bacteria?

Back 20

wet gangrene

Front 21

What type of necrosis is Wet Gangrene?

Back 21

liquifactive necrosis

Front 22

What can lead to Dry Gangrene?

Back 22

loss of blood supply to a limb

Front 23

What combination of necrosis causes Caseous Necrosis?

Back 23

Coagulative and liquifactive

Front 24

What commonly causes Caseous Necrosis?

Back 24

Tuberculosis and fungal infections

Front 25

What color are Caseous nodules?

Back 25

Pink

Front 26

What does the tissue look like in Caseous Necrosis?

Back 26

completely destroyed and structureless

Front 27

What can cause Fat Necrosis?

Back 27

the release of pancreatic lipase

Front 28

How can Fat Necrosis cause fat saponification?

Back 28

fatty acids combine with calcium

Front 29

What mineral do fatty acids combine with to cause saponification?

Back 29

calcium

Front 30

Where does Fibrinoid Necrosis occur?

Back 30

blood vessels

Front 31

What type of injury is Fibrinoid Necrosis associated with?

Back 31

immunological

Front 32

What happens to the Fibrin during Fibrinoid Necrosis?

Back 32

Fibrin in the plasma leaks out of the blood vessels

Front 33

What are the most common organs affected by atrophy?

Back 33

skeletal muscles, heart, secondary sex organs and the brain

Front 34

Inadequate supplies of what molecule results in ischemia consistent with atrophy?

Back 34

oxygen

Front 35

Interruption of what type of signal can cause atrophy?

Back 35

tropic (hormonal)

Front 36

What is an example of persistent cell injury that can lead to atrophy?

Back 36

chronic gastritis

Front 37

Define Hypertrophy.

Back 37

An increase in the size of the cells and consequently in the size of the affected organ.

Front 38

What organ is Hypertrophy common in?

Back 38

Heart (due to hypertension)

Front 39

What can lead to Hypertrophy?

Back 39

an increase in the amount of intracellular proteins

Front 40

What is Hyperplasia?

Back 40

an increase in the number of cells due to increased cellular division (can lead to increased organ size)

Front 41

Can hyperplasia and hypertrophy occur together?

Back 41

Yes, they are not mutually exclusive

Front 42

What type of cells cannot exhibit hyperplasia?

Back 42

Nerve, cardiac and skeletal muscle

Front 43

What mediates hyperplasia?

Back 43

growth factors, increased DNA synthesis and cellular division

Front 44

What are two hormones that cause hyperplasia?

Back 44

endogenous estrogen and EPO

Front 45

What are two factors that can increase functional demand and lead to hyperplasia?

Back 45

Increased bone marrow in high altitude and antigenic stimulation in lymphatic

Front 46

Define Metaplasia.

Back 46

reversible replacement of one mature cell by another that is better suited to tolerate the stress

Front 47

What happens in bronchial metaplasia?

Back 47

in smokers, columnar epithelium becomes squamous epithelium

Front 48

What occurs in acid reflux metaplasia?

Back 48

in the lower esophagus normal squamous epithelia become columnar epithelia

Front 49

Define dysplasia.

Back 49

Not a true adaptive change. It is an abnormal proliferation characterizied by changes in the size, shape and organization of mature cells

Front 50

Is dysplasia cancer?

Back 50

No, but it can lead to it.

Front 51

Is dysplasia a true adaptive change?

Back 51

No

Front 52

List the 11 causes of cell injury

Back 52

.Ischemia/hypoxia (most common type) , physical agents, burns/trauma, chemical agents, drugs poisons, nutritional, inadequate calorie, protein or excess vatamin deficiency, infectious diseases, viruses bacteria parasites, immunological mechanisms, hypersensitivity immunodeficiency or autoimmunity.

Front 53

List two cellular and subcellular changes in reversible injury

Back 53

cellular swelling and vacuole formation (decreased function of NaK ATPase), fatty change

Front 54

What changes due to reversible injury will show under electron microscope

Back 54

blebbing of the plasma membrane, swelling of mitochondria and clumping of chromatin, dilation of ER and dispersion of ribosomes

Front 55

When can irreversible injury occur

Back 55

mitochondrial damage (cell unable to make ATP), membrane is severely damaged, influx of calcium, nuclear changes, rupture of lysosomes

Front 56

What occurs during disruption of the plasma membrane

Back 56

massive influx of calcium

Front 57

What nuclear changes accompany irreversible injury

Back 57

pyknosis, karyorrhexis, and karyolysis

Front 58

define pyknosis

Back 58

the irreversible condensation of chromatin in the nucleus of a cell undergoing necrosis or apoptosis.

Front 59

define karyorrhexis

Back 59

destructive fragmentation of the nucleus of a dying cell whereby its chromatin is distributed irregularly throughout the cytoplasm

Front 60

define karyolysis

Back 60

the complete dissolution of the chromatin matter of a dying cell due to the activity of DNase

Front 61

What are the three mechanisms by which cells undero injury and death

Back 61

ATP depletion due to a loss of oxidative phosphorylation in the mitochondria, Loss of calcium homeostasis, reactive oxygen species

Front 62

What 5 steps occur during ATP depletion due to loss of oxidative phosphorylation in the mitochondria

Back 62

NaK pump fails and Na accumulates intracellularly, K diffuses out of the cell, Na Ca pump fails and Ca moves intracellularly, H2O and ions diffuse into the cell, Cell swells

Front 63

What occurs during a loss of calcium homeostasis

Back 63

Ca2+ influx due to energy failure of the ATP dependant calcium transporter will activate calcium dependant degradative enzymes

Front 64

Name the three ROS's

Back 64

hydrogen peroxide, superoxide anion, hydroxyl radicals

Front 65

What are three protective factors against free radicals

Back 65

Superoxide dismutase SOD, glutathione peroxidase GPx, Catalase

Front 66

What are the intracellular adaptations

Back 66

Fatty change, lipofuscin, hemosiderosis, cholesterol, calcification, hyaline changes

Front 67

Describe fatty change

Back 67

in alcoholic liver injury- reduced lipid export from liver cells and can no longer synthesize apoproteins

Front 68

describe lipofuscin

Back 68

wear and tear pigment, insoluble lipoprotein. Byproduct of lipid peroxidation and is nontoxic. Resists digestion and persists as membrane bound residual bodies

Front 69

describe hemosiderosis

Back 69

partially denatured form of ferritin- 25% of iron is stored in the form of ferritin and hemosiderin. Found in areas of hemorrhage and bruises. Normall in spleen , bone marrow and liver. When deposited systemically- hemosiderosis. In hemosiderosis as in frequent blood transfusion, iron present in organs where it is normally found and throughout the body, skin, pancreas, heart and kidney.

Front 70

Describe cholesterol

Back 70

muscle layer of heart blood vessel is filled with foam cells with lipid vacuoles

Front 71

What are the two types of calcification

Back 71

dystrophic and metastatic

Front 72

Where does Dystrophic calcification occur

Back 72

dead or injured cells

Front 73

what happens to blood calcium levels during Dystrophic calcification

Back 73

nothing, they remain normal

Front 74

what does Dystrophic calcification lead to

Back 74

crystal formation

Front 75

what is the microscopic appearance of Dystrophic calcification

Back 75

deep purple deposits in necrotic tissue

Front 76

where does Dystrophic calcification commonly develop

Back 76

aging or damaged heart valves

Front 77

do small deposits of calcium in necrotic tissue have clinical consequences

Back 77

no

Front 78

Where does metatstatic calcificaiton occur

Back 78

living cells or tissue

Front 79

what kind of calcium conditions occur during metatstatic calcificaiton

Back 79

hypercalcemic states

Front 80

what happens to serum calcium concentrations during metatstatic calcificaiton

Back 80

they increase

Front 81

What can cause metatstatic calcificaiton

Back 81

Vitamin D intox, multiple myeloma, parathyroid hormone, hyperparathyroidism, pagets disease

Front 82

Describe hyaline changes

Back 82

nonspecific term used to describe any intracellular or extracellular alteration that has pink homogenous appearance on an H and E stain

Front 83

what are some examples of hyaline changes

Back 83

alcoholic hyaline (intracellular), amyolid (extracellular), mallory bodies

Front 84

what are mallory bodies

Back 84

they are a type of intermediate filament between the size of actin and myosin

Front 85

What happens to cells during necrosis vs apoptosis

Back 85

necrosis- cell swelling apoptosis- cell shrinkage

Front 86

what happens to the nucleus or DNA during necrosis vs. apoptosis

Back 86

necrosis-- random nuclear fragmentation, apoptosis- specific DNA fragmentation

Front 87

does inflammation occur during necrosis vs. apoptosis

Back 87

necrosis- inflammation apoptosis- no inflammation