Inflammation

Front 1

Name the four responses to Cell Injury

Back 1

1. Adaptation
2. Cell Injury-irreversible and reversible
3. Intracellular Accumulations
4. Pathologic Calcification

Front 2

Adaptation to Cell Injury can include what? (Five things)

Back 2

Hypertrophy, atrophy, hyperplasia, metaplasia, and dysplasia.

Front 3

Increase in size of cells and consequently an increase in the size of the organ (can increase in size in response to an increased workload). Physiological or pathological

Back 3

Hypertrophy

Front 4

A response to injury by "downsizing" to conserve the cell.

Back 4

Atrophy

Front 5

True or False: Atrophy of cells means that they are dead.

Back 5

False: diminished function but they are not dead.

Front 6

An increase in the number of cells in an organ or tissue.

Back 6

Hyperplasia

Front 7

A reversible change in which one adult cell type is replaced by another adult cell type.

Back 7

Metaplasia

Front 8

Abnormality of development; Alteration in size, shape, and organization of adult cells.

Back 8

Dysplasia

Front 9

Insufficient oxygen to the tissues

Back 9

Hypoxia

Front 10

Causes of hypoxia: (3)

Back 10

Ischemia-arterial blood supply is interrupted.
Inadequate oxygenation of blood- as occurs in some lung diseases.
Inadequate oxygen-carrying capacity of blood- as occurs in anemia.

Front 11

There are four final common pathways related to the mechanisms of cell injury and death. What are they?

Back 11

1. Formation of oxygen-derived free radicals
2. Increase in intracellular concentration of Calcium
3. ATP depletion
4. Defects in membrane permeability

Front 12

Oxygen radicals are produced by _________ & ________.

Back 12

Neutrophils and radiation

Front 13

________ Respiration can not occur without the presence of oxygen, which contributes to the ATP depletion during hypoxia.

Back 13

Aerobic

Front 14

Name some common diseases in which cell injury and death would occur due to hypoxia.

Back 14

Myocardial Infarction
Stroke
Gangrene
ETC.....

Front 15

Cell death of living tissue

Back 15

Necrosis

Front 16

Type of necrosis: cell proteins denature, but the shape of the cell is maintained. Described as dead tissue with "tombstones" of the cells remaining.

Back 16

Coagulation Necrosis: can occur in muscle

Front 17

Type of Necrosis: Cell proteins denature but the shape of the cell is not maintained. Inflammatory cells influx and release digestive enzymes that liquify the involved tissue. The deaad cells form a semiliquid mass of material that is usually surrounded by viable tissue or fibrous tissue.

Back 17

Liquification Necrosis: occurs in the brain

Front 18

Type of necrosis: combination of coagulation and liquification necrosis that results in a cheese like shape. The dead tissue is found in the center of localized areas of inflammation called granulomas.

Back 18

Caseous Necrosis: occurs often from mycobacterial and fungal infections.

Front 19

Form of liquification necrosis that occurs when lipases digest fats in adipose tissues.

Back 19

Fat Necrosis

Front 20

One of the best microscopic indicators of tissue necrosis is loss of what?

Back 20

cell nuclei

Front 21

Disintegration of the nucleus occurs in a step fashion, what are the steps?

Back 21

Karyolysis- fading of the basophilia of nuclear chromatin (becomes redder)
Pyknosis- contraction of the nucleus with increased basophilia (nucleus becomes bluer)
Karyorrhexis-nucleus fragments.

Front 22

Programmed cell death

Back 22

Apoptosis

Front 23

Does inflammation normally occur with apoptosis.

Back 23

No

Front 24

Name two genes that are involved in apoptosis>

Back 24

bcl-2-necessary for apoptosis to occur, mutation leads to cell immortality
p53

Front 25

Three general forms of intracellular accumulations.

Back 25

1. normal cell component accumulates in excess.
2. abnormal substance accumulates due to a metabolic defect.
3. Accumulation of intracellular pigments or organisms.

Front 26

What is the "wear and tear" pigment?
Hint: composed of lipid and polymers, usually yellow and brown in color

Back 26

Lipofuscin

Front 27

Pigment formed from tyrosine i melanocytes; brown to black

Back 27

Melanin

Front 28

Composed of an aggregate of protein and ferric ions; formed when excess ferric ion is available in the microenvironment, such as hemorrhage and degradation of RBC; Yellow-brown

Back 28

Hemosiderin (larger than lipofuscin)

Front 29

Breakdown product of heme; may have a physical sign of jaundice.
Yellow-green.

Back 29

Bilirubin

Front 30

Exogenous pigment; Deposit in lungs when dust is inhaled. deposition in tissues can be described as anthracosis. Black.

Back 30

Carbon

Front 31

Calcium accumulation in cells that are injured or dead.

Back 31

Dystrophic calcification

Front 32

Calcium depostion in viable tissue usually due to a derangement in calcium homeostasis.

Back 32

Metastatic Calcification

Front 33

Three general forms of inflammation.

Back 33

Acute
Chronic
Granulomatous

Front 34

Signs and Symptoms of Acute inflammation (4).

Back 34

Redness(rubor)
Heat(calor)
Swelling(tumor)
Pain (dolor)

Front 35

What is the immediate vascular response to acute inflammation?

Back 35

There is an immediate, transient arteriolar constriction following injury.

Front 36

Following an immediate transient arteriolar constriction following injury, what comes next in the vascular changes?

Back 36

Precapillary arterioles then dilate and capillary beds open.
Capillary permeability increases, allowing protein-rich intravascular fluid to exude into the extracellular space.
Vasodilatoin and increased capillary permeability conspire to slow the local blood flow rate and cause vascular stasis.

Front 37

Neutrophils ______ in low flow rate capillaries where vascular stasis exists. The neutrophils then ______ to specific endothelial cell and basement membrane receptors.

Back 37

Marginate, adhere.

Front 38

Leukocytes actively squeeze through gaps between adjacent endothelial cells. They penetrate the capillary basement membrane by releasing enzymes that degrade the basement membrane, name the enzyme.

Back 38

Cathepsin

Front 39

When neutrophils are activated they either _______ or become _______.

Back 39

Degranulate, phagocytic

Front 40

What is opsonization?

Back 40

Coating of a bacteria or dead tissue (by IgG, C3b) so that is easily recognized by the leukocyte

Front 41

What enzyme catalyzes the formation of superoxide ions in the oxygen-dependent bactericidal mechanisms?

Back 41

NADPH oxidase

Front 42

Rare immunodeficiency characterized by a deficiency of NADPH oxidase in leukocytes.

Back 42

Chronic Granulomatous Disease

Front 43

Humoral mediator released from tissue mast cells that cause vasodilation and increased capillary permeability.

Back 43

Histamine and serotonin

Front 44

What does bradykinin do?

Back 44

Vasodilator and activate the coagulation system.

Front 45

Subtype of chronic inflammation that occurs when phagocytized material resists degradation within the phagolysosome.

Back 45

Granulomatous inflammation; calsed by some microorganisms, foreign material, autoimmune diseases(rheumatoid arthritis, rheumatic fever) and idiopathies (sarcoidosis).

Front 46

Four systemic effects of inflammation.

Back 46

1. fever- mediated by IL-1 and TNF.
2. Myalgia/Fatigue-IL-1 and TNF.
3. Leucocytosis-elevated WBC count.
4. Release of acute phase reactants from liver

Front 47

Main cell components in acute and chronic inflammation:

Back 47

Acute: Neutrophils, cytokines, and other mediators
Chronic: Macrophages and Lymphocytes, plasma cells

Front 48

True or false: Acute inflammation becomes chronic after it is present for an extended TIME period.

Back 48

False; dependent on cells present, not dependent on time.