Fund 2, Test 1

Front 1

What 3 things can occur after injury?

Back 1

Progression (further injury developing into chronic inflammation),

Healing (fibrosis and loss of function), and Resolution (return to normal function after clearance of injurous stimuli, mediators, and inflammatory cells)

Front 2

What are the cardinal signs of acute inflammation?

Back 2

Red (rubor),

Swelling (tumor),

Warm (calor),

tender (dolor),

loss of function (functio laesa)

Front 3

In what order do the inflammatory cells come to the site of injury?

Back 3

After edema comes the neutrophils (about 1 day) and then the monocytes/macrophages (about 2 days)

Front 4

What is a PMN?

Back 4

It is a polymorphonuclear lekocyte aka a neutrophil

Front 5

How does a neutrophil get into a site of injury?

Back 5

Margination (pavementing) and adhesion: so rolling, activation with chemokines, stable adhesion, then migration through endothelium.

Front 6

What are the mediators of emigration and chemotaxis?

Back 6

Bacterial products (LPS), Complement derivatives (C5a), arachidonic acid derivatives (leukotriene B4), and cytokines (IL-8)

Front 7

What comes from WBC defects?

Back 7

Chediak-higashi syndrome and diabetes mellitus

Front 8

What happens with chemotactic factor defects?

Back 8

C5 or immunoglobulin deficiency.

Front 9

What happens when there is a defect with the serum chemotaxis inhibitors?

Back 9

C5 inactivator defects cause an increase in cirrhosis, sarcoidosis, and other diseases.

Front 10

What happens when WBC locomotion inhibitors are defective?

Back 10

Chloroquine, cancer, and other chronic diseases can occur.

Front 11

What are the 3 steps of phagocytosis?

Back 11

Recognition, attachment, engulfment

Front 12

How does a cell recognize what its going to phagocytose?

Back 12

With opsoninzation (attachment of antibodies) and opsonins (Rc fragment of IgG, C3b, mannose-binding protein from liver) that cover the surface that allow it to be recognized.

Front 13

What happens after a macrophage attaches a bacteria it will phagocyize?

Back 13

It engulfs it and then merges it with a lysosome to degrade it with enzymes, NO, and reactive oxygen species.

Front 14

What is oxygen dependent killing?

Back 14

It is the use of reactive oxygen species such as HOCl and OH free radicals that is used to destroy a microorganism.

Front 15

How does a cell produce HOCl and OH free radicals?

Back 15

Myeloperoxidase uses hydrogen peroxide and halide (Cl-) to make HOCl, and Hydrogen peroxide and ferrous ion will generate OH free radical if myeloperoxidase is absent.

Front 16

What role does the liver play in the immune system?

Back 16

It produces the essential elements of coagulation (Factor XII – Hagerman factor) and inflammation (Complement activation – e.g. memgrane attack complex)

Front 17

What chemical mediators of inflammation are stored in secretory granules of mast cells, basophils, platelets, neutrophils, and macrophages?

Back 17

Histamine, serotonin, and lysosomal enzymes.

Front 18

Which chemical mediators of inflammation are newly synthesized?

Back 18

Prostaglandins, leukotrines, platelet-activating factors, activated oxygen specises, nitric oxide, and cytokines.

Front 19

Where does the arachidonic acid come from?

Back 19

Cell membranes

Front 20

What are some things that can be produced from arachidonic acids?

Back 20

Prostaglandins, leukotrines, lipotoxins, and other inflammatory mediators. They affect vasoconstriction/dialation, chemotaxis, edema, etc.

Front 21

What is transudate?

Back 21

Fluid with low protein content and a specific gravity <1.012

Front 22

What is Exudate?

Back 22

Inflammatory extracellular fluid composed of plasma proteins, principally albumin, cells and cellular debris, and a specific gravity >1.020.

Front 23

What is Anasarca?

Back 23

Edema which is severe and generalized

Front 24

What is an abcess?

Back 24

Localized collections of pus caused by suppuration buried in a tissue, organ, or confined space.

Front 25

What is cellulitis?

Back 25

Spreading suppurations in subcutaneous tissue.

Front 26

Name the types of exudates and an example of each.

Back 26

Serous – blister;

Fibrinous – uremic pericarditis, viral/chemical pneumonitis;

Purulent – meningococcal meningitis; Eosinophilic – asthma and parasitic infections (IgE mediated);

Hemorrhagic – rickettsial;

pseudomembranous – diptheria and pseudomembranous enterocolitis.

Front 27

What does this picture show?

Back 27

Pulmonary edema with transudate.

Front 28

What does this image show?

Back 28

Ascites: the accumulation of fluid in the peritoneal cavity, causing abdominal swelling.

Front 29

This is an example of:

Back 29

Fibrinous pericarditis.

Front 30

What type of acute inflammation is this?

Back 30

Purulent: you can see its filled with cells and the remains of cells - pus = dead white blood cells.

Front 31

What type of exudate is this?

Back 31

Pseudomembranous, specifically from diphtheria.

Front 32

What is this? What are the arrows pointing to?

Back 32

This is hydropic degeneration: The accumulation of water in a cell that usually leads to cell death.

Red arrow: dead heart cells

Black arrow: Hydropic degeneration, reversible swelling. Still alive, but not healthy.

Blue arrow: Normal heart cells.

Front 33

What type of necrosis is this?

Back 33

Coagulative Necrosis.

Front 34

What type of necrosis is this?

Back 34

Liquefaction necrosis.

Front 35

What type of necrosis is this?

Back 35

Liquefaction.

Front 36

What are the tiny bumps?

Back 36

Pancreatic fat necrosis

Front 37

What type of necrosis is this?
What disease could have caused this?

Back 37

This is caseous necrosis caused by TB.

Front 38

What is this?

Back 38

Caseous necrosis

Front 39

What type of necrosis is this?

Back 39

fibrinoid necrosis

Front 40

What type of necrosis is this?

Back 40

Gangrenous necrosis.

Front 41

What is this an example of?

Back 41

squamous metaplasia.

Front 42

What is this an example of?

Back 42

Prostatic hyperplasia

Front 43

What is this?

Back 43

This is disuse atrophy.

Front 44

What is this?

Back 44

This is fatty change in the liver stained with Oil Red O stain.

Front 45

What is this?

Back 45

Alcoholic hyalin

Front 46

What is this?

Back 46

Anthracosis

Front 47

What is this?

Back 47

Metastatic calcification

Front 48

What is this?

Back 48

dystrophic calcification.

Front 49

What is this?

What could have caused it?

Back 49

Granulomatous Inflammation that could be caused by TB.

Front 50

What is this?

Back 50

A closeup of granulomatous inflammation. Note the epithelioid macrophages.

Front 51

What is this?

Back 51

This is an excessive wound repair known as a keloid. It is made of fibrinous tissue.

Front 52

What is this? What disease is it associated with?

Back 52

This is a petechiae rash and is associated with Meningococcal Meningitis.

Front 53

What is this? What disease is it associated with?

Back 53

This is a purpura rash (formed when the splotches from the petechiae accumulate) and is associated with Meningococcal Meningitis.

Front 54

What are the 4 main types of cell adaptation?

Back 54

Atrophy, hypertrophy, hyperplasia, metaplasia.

Front 55

What are the 2 possible outcomes from an irreversible injury? What is the main difference between them?

Back 55

Necrosis and apoptosis. Necrosis involves inflammation whereas apoptosis does not.

Front 56

Define Hypoxia and Ischemia.

Back 56

Hypoxia: decreased availability of oxygen (pneumonia) and/or loss of oxygen carrying capacity of blood (anemia).

Ischemia: Insufficient blood supply, often caused by occlusion of artery or vein.

Front 57

What is troponin I?

Back 57

It is a protein released by dying heart cells.

Front 58

What are the results of oxygen depravation?

Back 58

The mitochondria cannot use oxidative phosphorylation which leads to: ER swelling, cellular swelling, loss of microvilli, blebs, clumping of nuclear chromatin (due to low pH from buildup of lactic acid), and lipid deposition.

Front 59

What are the signs of a reversible injury?

Back 59

Cell swelling leading to hydropic change or vacuolar degeneration.

Front 60

What happens with an irreversible injury?

Back 60

Cell death leading to necrosis. Also, nuclear pyknosis followed by karyorrhexis and karyolysis.

Front 61

What are pyknosis, karyorrhexis, and karyolysis?

Back 61

They are the steps in the destruction of genetic material.

Pyknosis: shrinking of chromosomes

Karyorrhexis: breaking up of nucleus

Karyolysis: all pieces of nucleus dissolve away.

Front 62

Why do dead cells appear so bright on histology slides?

Back 62

The build up of lactic acid as the cells died causes the degeneration and coagulation of proteins which allows the stain to bind really well.

Front 63

How can ROS be generated?

Back 63

Redox reactions, absorption of radiant energy, in activated leukocytes during inflammation, enzymatic metabolism of exogenous chemicals/drugs, transition metals (iron and copper), nitric oxide and peroxynitrite anion.

Front 64

How do cells remove ROS?

Back 64

Antioxidants (vitamins E, A, C, and glutathione)

Iron and copper binding proteins (transferrin, ferritin, lactoferrin, and ceruloplasmin)

Enzymes (catalase, superoxide dismutases, glutathione peroxidase)

Front 65

What are the pathologic effects of ROS?

Back 65

Lipid peroxidation in membranes (they become stiff and break), oxidative modification of proteins, DNA damage.

Front 66

Define coagulative necrosis.

Back 66

Dissolution of nucleus with preservation of cellular shape and tissue architecture, also coagulation (denaturation) of cell proteins. It appears to leave behind a "ghost" of the cell.

Front 67

Define liquefaction necrosis.

Back 67

Hydrolytic enzymes cause autolysis and heterolysis (liquefaction) of cells/tissues. Begins as coagulation, but then the cells break apart into mush. It is the complete degradation of cells down to the molecular level.

Front 68

What are the components of pus?

Back 68

neutrophils, bacteria, and dead tissue.

Front 69

What is fat necrosis?

Back 69

Destruction of adipose tissue due to the action of lipases: happens especially in liver and pancreas.

The lipase reacts to lipids, releases free fatty acids that react with calcium in the blood to make salts: saponification.

Front 70

What is caseous necrosis?

Back 70

A combination of coagulative and liquefaction necrosis that is primarily found in the center of tubercles. It is the result of an inability to digest and remove material from center of granuloma.

Front 71

What is fibrinoid necrosis?

Back 71

Necrotic tissue due to immunologic reaction. It is usually seen in blood vessels with deposition of complement and antibodies in vessel wall (e.g. kidney)

Front 72

What is gangrenous necrosis?

Back 72

It is coagulative necrosis with a secondary bacteria infection that leads to liquefaction.

Front 73

What are the 2 forms of gangrenous necrosis?

Back 73

Dry gangrene: coagulative necrosis is predominant pattern. Usually when there isn't enough blood for lots of liquefaction.

Wet gangrene: liquefactive process is the dominant pattern. Usually when there is plenty of blood available.

Front 74

What are the 2 types of apoptosis?

Back 74

Physiologic apoptosis: embryogenesis and hormone-dependent involution (e.g. menstrual cycle)

Pathologic apoptosis: viral diseases and injurious agents leading to cell death.

Front 75

What are the mechanisms for apoptosis?

Back 75

Activation of endonuclease, cytoskeleton disruption by proteases, cytoplasmic protein cross-linking by transglutaminase, and cell surface changes leading to phagocytosis.

Front 76

What are the morphologic characteristics of apoptosis?

Back 76

General cell shrinkage, chromatin condensation, bleb formation and apoptotic bodies, phagocytosis, and lack of an inflammatory reaction.

Front 77

Define atrophy.

Back 77

Shrinkage in the size of the cell by loss of structural components. This may be due to decreased work load, loss of innervation, diminished blood supply, inadequate nutrition, loss of endocrine stimulation.

Front 78

Define hypertrophy.

Back 78

Increased size of cells and the organ. Can be physiologic (hormonal stimulation like uterus) or pathologic (increased functional demand e.g. left ventricular hypertrophy (LVH))

Front 79

Define hyperplasia.

Back 79

Increase in the number of cells in an organ or tissue. Can be physiologic (hormone induced like breast in pregnancy) or pathologic (viral induced or excessive hormonal stimulation).

Front 80

Define metaplasia.

Back 80

Reversible change in which one differentiated cell type is replaced by another cell type.

Front 81

True/False: An example of metaplasia is ciliated columnar epithelium turning directly into squamous epithelium.

Back 81

False! The ciliated columnar do not turn into squamous epithelium. It is the stem cells that will begin forming the squamous to replace the columnar as they die. A ciliated columnar epithelium cannot change directly into a squamous epithelium.

Front 82

Give an example of when metaplasia would occur.

Back 82

If a kidney stone continually rubbed up against the columnar epithelium of the kidney, then the kidney would develop squamous epithelium to prevent/mitigate the damage.

Front 83

True/False: Metaplasia is reversible.

Back 83

True.

Front 84

Name some normal and abnormal cellular constituents than can abnormally accumulate in a cell.

Back 84

Normal: lipids, proteins, glycogen, carbohydrates.

Abnormal: carbon, silica, asbestos, bacteria.

Front 85

What is fatty change?

Back 85

It is when the amount or distribution of fat changes. So too much lipid going in or not enough coming out.

Lipid in macrophages: foam cells - atherosclerosis

Lipid in parenchyma cells: alcoholic fatty liver.

Front 86

What are hyaline droplets?

Back 86

Accumulation of intracellular proteins, especially in the kidney proximal tubules.

Front 87

Where can you find Russell bodies?

Back 87

In plasma cells.

Front 88

What is alcoholic hyaline?

Back 88

A poorly defined accumulation of eosinophilic material in the cytoplasm of damaged liver cells in certain forms of cirrhosis. Looks like tangled skeins of cytokeratin intermediate filaments and other proteins. Also called Mallory Alcoholic hyaline.

Front 89

What are some exogenous pigments?

Back 89

Carbon (anthracosis)

tattooing

natural substances (beta carotene)

poisons (Lead: Pica)

Front 90

What are some endogenous pigments?

Back 90

Lipofuscin, melanin, and hemosiderin.

Front 91

What is hemosiderosis and hemochromatosis?

Back 91

Hemosiderosis: iron overload in phagocytic cells, no tissue damage.

Hemochromatosis: iron overload in parenchymal (functional, not structural) cells, tissue damage occurs.

Front 92

What is metastatic calcification?

Back 92

Deposition of calcium in normal tissues due to hypercalcemia. Often found in interstitial tissues of blood vessels, kidneys, lungs, and gastric mucosa.

Front 93

What is dystrophic calcification?

Back 93

Deposition of calcium salts in necrotic tissues. Can be intracellular, extracellular or both. Heterotopic bone may form with time.

Front 94

What are the different types of fixed macrophages and where are they found?

Back 94

Kupffer cells - liver

histiocytes - connective tissue

microglia - brain

osteoclasts - bone

Langerhans cells - epidermis.

Front 95

What is granulomatous inflammation?

Back 95

Focal accumulations of activated macrophages with an epithelial-like (epithelioid) appearance.

Front 96

What is a granuloma?

Back 96

A microscopic aggregation of epithelioid macrophages surrounded by a collar of lymphocytes and occasionally plasma cells.

Front 97

What is granulation tissue?

Back 97

It is the proliferation of new blood vessels and fibroblasts. Fibroblasts turn into myofibroblasts.

Front 98

In general terms, what is the order of healing?

Back 98

Inflammation, formation of granulation tissue (when inflammation ends, collagen accumulation begins), and then finally wound contraction.

Front 99

What is primary union wound healing?

Back 99

Healing by first intention: The healing of a clean surgical incision. Very little tissue damage is present.

Front 100

What is secondary union wound healing?

Back 100

Healing by second intention: The healing of a large tissue defect such as road rash.

Front 101

Which is quicker, primary union or secondary union and why?

Back 101

Primary union is quicker because it is easier to pull the small incision together than it is with a large scrape.

Front 102

What are some of the causes of wound healing abberations?

Back 102

Inadequate granulation tissue/healing, excessive repair (hypertropic scar or keloid), contractures (shortening and hardening of muscles).

Front 103

What are some conditions that would inhibit or delay wound healing?

Back 103

Poor local vascular supply (poor oxygenation, decreased bacterial resistance, low temperature, and acidic pH)

Deficiencies of vitamin C, protein, zinc

Infecton

Tissue necrosis (foreign materal delay healing and acts as a nidus for bacterial infection

Excessive movement.

Front 104

What is the main component of the extracellular matrix?

Back 104

Collagen. Specifically extra cellular which is after the procollagen has been cleaved and the lysine oxidized to promote cross-linking. It has very high tensile strength.

Front 105

What will allow the maximal tensile strength of 70 to 80% of normal?

Back 105

The replacement of Type III collagen with Type I in wound healing.

Front 106

What will lead to fibrosis (tissue scar)?

Back 106

Persistent tissue damage such as chronic inflammatory diseases (cirrhosis, chronic pancreatitis, pulmonary fibrosis)

Front 107

What is associated with acute injury?

Back 107

Vasoconstriction/dilation, fluid and protein leakage into interstitium (exudate), neutrophils (transudate), monocytes/macrophages cleaning up mess (phagocytosis)

Front 108

What is associated with chronic injury?

Back 108

Macrophages (cleaning up and recruiting more/proliferating), lymphocytes (regulating macrophages, orchestrating healing), granulomatous inflammation and/or granulomas.

Front 109

What is associated with healing?

Back 109

Macrophages (still cleaning up, becoming mature for that tissue), early granulation tissue (fibroblasts), early fibrosis (Type III collagen, myofibroblasts), collagen maturation (to Type I), and scar (with 70% of tensile strength).