Pathology Test 1 2011

Front 1

Define the term “pigment” as it applies to pathology.

Back 1

A substance that has its own color despite/even with staining.

**Most tissues are colorless.

Front 2

Distinguish “endogenous” from “exogenous” pigments, and provide typical examples of each.

Back 2

* Endogenous- origin within the patient (melanin)

* Exogenous- origin outside the patient (pneumoconiosis)

Front 3

Describe the biological derivation of lipofuscin.

Back 3

** A wear and tear pigment/aging pigment- lipid derived pigment (oxidative breakdown or injury to membrane lipids) finely granular, intracytoplasmic golden brown deposit


** Commonly seen in aged cells, chronically injured cells- indicates prolonged or increased rate of lipid oxidation and turnover

Front 4

Describe the biological derivation and pathological significance of hemosiderin.

Back 4

Ferritin (iron storage protein) gets old, sticky, and insoluble and precipitates within the cell as hemosiderin (can see as golden brown pigment in tissue- indicates an area of a lot of iron storage (site of previous hemorrhage or in spleen/liver where RBCs are broken down)

Front 5

What is hemosiderin?

Back 5

Hemosiderin is insoluble deposits of denatured ferritin

Front 6

Describe the general physiologic pathways for creation and elimination of bile pigments.

Back 6

1. Local bruise/injury leads to a loss of blood from vessels into surrounding tissues

2. Erythrocytes are ingested by tissue-resident macrophages

3. Pigments are derived from heme breakdown (heme is turned into linear products and iron and globin is turned into amino acids and reused)

4. Bile pigments (bilirubin and biliverdin) which are linear products of heme breakdown begin to accumulate at site of hemorrhage

5. The bile pigments are carried on plasma protein albumin to liver

6. Hepatic conjugation and excretion of bile pigments

Front 7

What is icterus?

Back 7

Yellow discoloration of tissues due to excess systemic, circulating bile pigments

Front 8

How does icterus occur?

Back 8

Occurs because of excessive erythrocyte destruction (hemolytic diseases) or impaired bile secretion (physically obstructed bile duct, impairment of hepatocellular bile pigment metabolism, impairment of hepatocellular bile pigment excretion)

Front 9

What is melanosis?

Back 9

Excessive melanin accumulation within a tissue

** Usually unexpected but otherwise normal

Front 10

What is pseudomelanosis?

Back 10

* False melanosis- actually a post mortem reaction of microbial H2S with iron in tissues

* Makes Iron Sulfide which is a black pigment; usually occurs when H2S diffuses from bowel into organ

Front 11

What is albinism?

Back 11

* Lack of melanin (usually a tyrosinase deficiency and usually inherited)

* Can have tyrosinase-negative albinism or tyrosine positive albinism (another enzyme in the process is affected)

Front 12

What is hemosiderosis?

Back 12

* A condition of having excess hemosiderin

** Occurs at site of previous hemorrhage or sites of erythrophagocytosis like the liver and spleen

Front 13

Define pneumoconiosis, and distinguish it from anthracosis

Back 13

* Pneumoconiosis: a general term for any and all pigmentations of lung by inhaled, fine particulate matter.

* Anthracosis: specifically refers to pneumoconiosis that specifically refers to carbon dust.

Front 14

What is the smallest size object you can see with a light microscope?

Back 14

Usually you can’t see anything that is less than 0.25 micrometers with a light microscope

Front 15

Describe the usual methods used to histologically distinguish lipid, glycogen, and water.

Back 15

1. Lipid- lost in routine processing of tissue so it won’t stain because it isn’t even there (will just look like water because water fills in spaces where lipid was)

* To see lipid you must get a frozen section and stain it for “oil red o” which stains lipids

2. Water- ubiquitous in tissue, stains, etc. so there are no distinguishing features when it is in vacuoles

3. Glycogen- persists in routinely processed tissues

* Stains with periodic acid Schiff’s reagent (stains magenta)

Front 16

Describe the 2 fundamental pathways to lethal cellular injury. Provide practical examples of both mechanisms.

Back 16

1. Interference with cellular energy metabolism

* Hypoxia, disruption of electron transport (cyanide), lack of energy source (hypoglycemia)

2. Damage to cell membrane

* Enzymatic destruction (bacterial phospholipases); physical trauma; oxidant-mediated membrane damage (free radicals)

Front 17

Describe the major cellular mechanisms for generating free radicals.

Back 17

1. Partial reduction of oxygen by “respiratory chain” (instead of producing water and energy you generate intermediates like superoxide, hydrogen peroxide, and hydroxyl ions)

2. Lysis of water by ionizing radiation or reaction with metals

3. Cellular oxidase systems like cytochrome P450, xanthine oxidase and NADPH oxidase

Front 18

Describe how to prevent or limit free radical-mediated injury.

Back 18

1. Antioxidants such as vitamin E

2. Sulfhydryl compounds such as glutathione + glutathione peroxidase
(selenium is important for function of peroxidase)

3. Superoxide dismutase

Front 19

Describe the usual biochemical targets of free radical-mediated injury in cells.

Back 19

Free radicals can injure cell membranes (fatty acid oxidation, lipid-lipid crosslinks, damage to membrane associated proteins such as strand cleavage and disulfide linkages) or nucleic acids (DNA nucleotide damage)

Front 20

6. Describe the major pathologic mechanisms for accumulation of excess lipid in cells.

Back 20

Anything that increases rate of entry of fatty acids into the fatty acid pool or decreases rate of exit (thus increasing or decreasing the amount of triglycerides in the cytosol which is how lipids are stored if there is excess)

Front 21

What are some ways to increase the rate of lipids in cells?

Back 21

1. More fatty acids in diet

2. More fatty acids mobilized from neutral fat stores

3. De novo synthesis of fatty acids from acetate

4. Synthesis of triglycerides from alpha-glycerophosphate

Front 22

What are some ways to decrease the rate of lipids in cells?

Back 22

1. Decreased rate of lipoprotein production

2. Decreased conversion of triglycerides back to fatty acids where they can then be oxidized or incorporated into phospholipids or cholesterol esters

Front 23

What is necrosis?

Back 23

Non-physiological cell death within a living tissue

Front 24

9. Describe the typical histologic changes commonly associated with lethal cell injury and cell death.

Back 24

1. Cytoplasmic changes- cytoplasmic staining altered (increased eosinophilia); vacuolation may be severe; loss of normal granularity (hyalinization)


2. Nuclear changes- nuclear shrinkage and increased basophilia (pyknosis); eventual fragmentation of chromatin (karyorrhexis); dissolution of chromatin (karyolysis)

Front 25

What are the 3 types of necrosis?

Back 25

Coagulative, caseous, liquefactive

Front 26

What is coagulative necrosis?

Back 26

* Preservation of overall tissue architecture

* Cellular detail is lost but cellular outlines may still be visible (can still ID tissue; usually occurs with abrupt interruption in blood flow, etc. so that cells are killed rapidly)

Front 27

What is caseous necrosis?

Back 27

* Cells dead and tissue architecture is liquefied so tissue is not recognizable

* Enzymatic destruction of dead tissue; neutrophils and other inflammatory cells can be sources of destructive enzymes along with bacterial agents who provide their own destructive enzymes

Front 28

What is liquefactive necrosis?

Back 28

“cheese like” dead cells and tissue architecture is lost


* Tissue takes gross appearance for dry cottage cheese (common in TB lesions)

Front 29

What is apoptosis?

Back 29

Apoptosis- programmed cell death

** Cells get a signal to die and then through a series of energy requiring steps they do