CHAPTER 2 (Cellular Responses to Stress)

Question 1

Study of the structural, biochemical, and functional chnages in cells, tissues, and organs that underlie disease

Answer 1

Pathology

Question 2

Study of the causes, mechanisms, and morphologicc and biochemical correlates of cell injury.

Answer 2

Pathology

Question 2

Pathology is divided into:

Answer 2

(1) General Pathology
(2) Systemic Pathology

Question 3

This determines morphologic and clinical patterns of disease

Answer 3

Injury to cells and to extracellular matrix (which ultimately leads to tissue and organ injury)

Question 3

4 Aspects of a Disease Process that form the Core of Pathology:

Answer 3

1. Cause or Etiology
2. Pathogenesis
3. Morphologic Changes
4. Clinical Manifestations

Question 3

These are the factors that cause the disease and are categorized either as genetic or acquired

Answer 3

Cause or Etiology

Question 3

Enumerate the Cause or Etiology that are Genetic

Answer 3

• Inherited mutations
• Disease Associated Gene Variants
• Polymorphisms

Question 3

Enumerate the Cause or Etiology that are Acquired

Answer 3

• Infections
• Nutritional
• Chemical
• Physical

Question 3

Also knownss as Diagnostic Cornerstone

Answer 3

Pathogenesis

Question 4

Described as biochemical and molecular mechanisms of its development

Answer 4

Pathogenesis

Question 4

Remains as one of the main domains of pathology.

It is a sequence of cellular, biochemical, and molecular events that follow the exposure of cells or tissues to an injurious agent

Answer 4

Pathogenesis

Question 4

Structural alterations induced in the cells and organs of the body

Answer 4

Morphologic Changes

Question 4

The end results of genetic, biochemical, and structural changes in cells and tissues are functional abnormalities, which lead to the clinical manifestations (symptoms & signs) of disease, as well as its progress (clinical course and outcome)

Answer 4

Clinical manifestations

Question 4

What is the cellular response if the injurious stimuli are increased demand, increased stimulation?

Answer 4

Cellular adaptations such as Hyperplasia & Hypertrophy

Question 5

Form of cell death, hybrid

Answer 5

Necroptosis

Question 5

Enumerate the characteristics of necroptosis that resembles necrosis

Answer 5

1. Loss of ATP
2. Swelling of cell and organelles
3. Generation of ROS
4. Release of lysosomal enyzmes
5. Rupture of the plasma membrane

Question 5

Cite the characteristic of necroptosis that resembles apoptosis

Answer 5

Triggered by genetically programmed signal transduction events that culminate cell death

Question 5

Sometimes called programmed necrosis, or “caspase-independent” programmed cell death

Answer 5

Necroptosis

Question 5

Process in which a cell eats its own contents

Answer 5

Autophagy

Question 6

It involves the delivery of cytoplasmic materials to the lysosome for degradation

Answer 6

Autophagy

Question 6

Three types of Autophagy depending on how the materils are delivered

Answer 6

1. Chaperone-mediated autophagy
2. Microautophagy
3. Macroauthophagy

Question 6

Direct translocation across the lysosomal membrane by chaperone proteins

Answer 6

Chaperone-mediated autophagy

Question 6

Inward invagination of lysosomal membrane for delivery

Answer 6

Microautophagy

Question 6

The major form of autophagy involving the sequestration and transportation of portions of cytosol in a double membrane bound autophagic vacuole (autophagosome)

Answer 6

Macroauthophagy

Question 7

It is implicated in many physiologic states (such as aging and exercise) and pathologic processes

Answer 7

Autophagy

Question 7

Components of the myelin figures found in necrotic cells

Answer 7

Phospholipids

Question 8

Abnormal accumulations of triglycerides within the parenchymal cells

Answer 8

Steatosis (fatty change)

Question 9

Fatty change is often seen in the _____ because it is the major orgna involved in fat metabolism, but it also occurs in ___________

Answer 9

liver; heart, muscle, and kidney

Question 10

Causes of steatosis

Answer 10

toxins, protein malnutrition, DM, obesity, anorexia

Question 11

Accumulations manifested histologically by intracellular vacuoles

Answer 11

Cholesterols and Cholesterol esters

Question 12

In this pathologic process, smooth muscle and macrophages within the intimal layer of the aorta and large arteries are filled with lipid vacuoles

Answer 12

Atherosclerosis

Question 13

Appearance of the cells in athrosclerosis

Answer 13

**Foamy appearance** (foam cells) and aggregates of them in the intima produce **yellow cholesterol-laden atheromas**

Question 14

Intracellular accumulation of cholesterol within macrophages

Answer 14

Xanthomas

Question 15

Focal accumulations of cholesterol-laden macrophages in the lamina propria of the gallbladder. The mechanism of accumulation is unknown

Answer 15

Cholesterolosis

Question 15

Clusters of foamy cells are found in the **subepithelial connective tissue of the skin and in tendons** producing tumorous masses

Answer 15

Xanthomas

Question 16

**Lysosomal storage disease** caused by mutations affecting an enzyme involved in cholesterol trafficking, resulting in cholesterol accumulation in multiple organs

Answer 16

Niemann- Pick disease, type C

Question 17

Intracellular accumulations of proteins usually appear?

Answer 17

rounded, eosinophilic droplets, vacuoles, or aggregates in the cytoplasm

Question 18

By electron microscopy, proteins appear?

Answer 18

amorphous, fibrillar, or cystalline

Question 18

Seen in renal diseases associated with protein loss in the urine (proteinuria)

Answer 18

Reabsorption droplets in proximal renal tubules: nephrotic syndrome

Question 18

In this disorder, abnormal proteins deposit primarily in extracellular spaces

Answer 18

Amyloidosis

Question 19

Excesses of Proteins Within the Cells Sufficient to Cause Morphologically Visible Accumulation have Diverse Causes such as:

Answer 19

1. Reabsorption droplets in proximal renal tubules: nephrotic syndrome 2. Production of excessive amounts of normally secreted proteins: multiple myeloma (russell bodies) 3. Detective intracellular transport and secretion of critical proteins: a1-antitrypsin deficiency 4. Accumulation of cytoskeletal proteins: Alzheimer's disease (neurofibrillary tangles) 5. Aggregation of abnormal proteins: Amyloidosis

Question 19

In the kidney, small amounts of protein filtered through the glomerulus are normally reabsorbed by _______ in the proximal tubule

Answer 19

pinocytosis

Question 19

Occurs in certain plasma cells engaged in active synthesis of immunoglobulins.

Answer 19

Production of excessive amounts of normally secreted proteins: multiple myeloma (russell bodies)

Question 20

The ER becomes hugely distended, producing large, homogenous eosinophilic inclusions called?

Answer 20

Russell Bodies

Question 20

Mutations in the protein significantly slow folding, resulting in the buildup of partially folded intermediates which aggregate in the ER of the liver and are not secreted

Answer 20

Detective intracellular transport and secretion of critical proteins: a1-antitrypsin deficiency

Question 21

What are the several types of cytoskeletal proteins?

Answer 21

1. Microtubules (20-25 nm) 2. Thin actin filaments (6-8 nm) 3. Thick myosin filaments (15 nm) 4. Intermediate filaments (10 nm)

Question 22

Provide a flexible intracellular scaffold that organizes the cytoplasm and resists forces applied to the cell

Answer 22

Intermediate filaments

Question 22

Five classes of intermediate filaments:

Answer 22

1. Keratin filaments (epithelial cells) 2. Neurofilaments (neurons) 3. Desmin filaments (muscle cells) 4. Vimentin filaments (connective tissue cells) 5. Glial filaments (astrocytes)

Question 23

These disorders are sometimes called proteinopathies or protein-aggregation disease

Answer 23

Aggregation of abnormal proteins: amyloidosis

Question 24

Usually refers to an alteration within cells or in the extracellular space that gives a homogeneous, glassy, pink appearance

Answer 24

Hyaline change

Question 25

Produced by a variety of alterations and does not represent a specific patterin of accumulation

Answer 25

Hyaline change

Question 26

Intracellular hyaline

Answer 26

- Reabsorption droplets - Russell bodies - Alcoholic hyaline

Question 27

Extracellular hyaline

Answer 27

- Collagenous fibrous tissue in old scars - Walls of arteioles in long-standing hypertension and DM

Question 28

Readily available energy source stored in the cytoplasm of healthy cells

Answer 28

Glycogen

Question 28

Whatever the clinical setting, the glycogen masses appear as ________ within the cytoplasm

Answer 28

clear vacuoles

Question 29

Prime example of a disorder of glucose metabolism. In this disease glycogen is found in renal tubular epithelial cells, as well as within liver cells, B cells of the islet of langerhans, and heart muscle cells

Answer 29

Diabetes mellitus

Question 29

Dissolves in aqueous fixatives, most readily identified when tissus are fixed in absolute alcohol

Answer 29

Glycogen

Question 29

In these diseases, enzymatic defects in the synthesis or breakdown of glycogen result in massive accumulation, causing cell injury and cell death

Answer 29

Glycogen storage disease or Glycogenoses

Question 29

What stain is used to stain glycogen that imparts a rose-to-violet color

Answer 29

Best Carmine or PAS reaction

Question 30

Exogenous pigments

Answer 30

1. Carbon (Coal dust) 2. Tattooing

Question 30

Most common exogenous pigment. Ubiquitous air pollutant in urban areas

Answer 30

Carbon (Coal dust)

Question 30

Accumulations of this pigment blacken the tissues of the lungs (Anthracosis) and the involved lymph nodes

Answer 30

Carbon (coal dust)

Question 31

A form of localized, exogenous pigmentation of the skin

Answer 31

Tattoing

Question 31

Carbon dust may induce a fibroblastic reaction or even emphysema and thus cause a serious lung disease known as

Answer 31

Coal Worker's Pneumoconiosis

Question 32

The pigments do not usually evoke any inflammatory response

Answer 32

Tattoing

Question 33

Endogenous Pigments

Answer 33

1. Lipofuscin 2. Melanin 3. Homogentisic acid 4. Hemosiderin

Question 33

An insoluble pigment also known as lipochrome or wear-and-tear pigment

Answer 33

Lipifuscin

Question 33

Not injurious to the cell or its functions. Its importance lies in being a telltale sign of free radical injury and lipid peroxidation

Answer 33

Lipofuscin

Question 33

In tissue sections it appears as a yellow-brown, finely granular cytoplasmic, often perinuclear, pigment

Answer 33

Lipofuscin

Question 33

It is seen in cells **undergoing slow, regressive changes** and is particularly prominent in the liver and heart of aging patients or patients with sever malnutrition and cancer cachexia

Answer 33

Lipofuscin

Question 33

It is the **only** endogenous brown-black pigment

Answer 33

Melanin

Question 33

An endogenous, brown-black pigment formed when the enzyme **tyrosinase** catalyzes the oxidation of tyrosine to dihydroxyphenylalanine in melanocytes

Answer 33

Melanin

Question 33

Black pigment that occurs in patients with alkaptonuria, a rare metabolic disease

Answer 33

Homegentisic acid

Question 33

A hemoglobin-derived, golden yellow to brown, granular or crystalline pigment. One of the major storage forms of iron

Answer 33

Hemosiderin

Question 33

Represents aggregates of ferritin micelles

Answer 33

Hemosiderin

Question 34

Best example of localized hemosiderosis

Answer 34

common bruise

Question 34

When there is systemic overload of iron hemosiderin may be deposited in many organs and tissues, a condition called

Answer 34

Hemosiderosis

Question 34

Abnormal tissue deposition of calcium salts, together with smaller amounts of iron, magnesium, and other mineral salts

Answer 34

Pathologic calcification

Question 34

Two forms of pathologic calcification

Answer 34

1. Dystrophic calcification 2. Metastatic calcification

Question 34

When the deposition occurs locally in dying tissues

Answer 34

Dystrophic calcification

Question 34

It occurs despite normal serum levels of calcium and in the absence of derangements in calcium metabolism

Answer 34

Dystrophic calcification

Question 34

Deposition of calcium salts in otherwise normal tissues

Answer 34

Metastatic calcification

Question 34

It almost always results from **hypercalcemia** secondary to some disturbance in calcium metabolism

Answer 34

Metastatic calcification

Question 34

Encountered in areas of necrosis, whether they are of coagulative, caseous, or liquefactive type, and in foci of enzymatic necrosis of fat

Answer 34

Dystrophic calcification

Question 35

Almost always present in the atheromas of advanced atherosclerosis

Answer 35

Dystrophic calcification

Question 36

Although it may simply be a telltale sign of previous cell injury, it is **often a cause of organ dysfunction**

Answer 36

Dystrophic calcification

Question 36

This blood test is normal in Dystrophic calcification

Answer 36

Serum calcium

Question 37

The progressive acquisition of outer layers may create lamellated configurations called

Answer 37

Psammona bodies

Question 37

Appear microscopically as **fine, white granules or clumps**, often felt as **gritty deposits**

Answer 37

Calcium salts

Question 38

Over time, this may be formed in the focus of calcification

Answer 38

Heterotopic bone

Question 39

It also accentuates dystrophic calcification

Answer 39

Hypercalcemia

Question 39

Four principal cause of hypercalcemia:

Answer 39

1.) Increased secretion of parathyroid hormone (PTH) with subsequent bone resorption 2.) Resorption of bone tissue 3.) Vitamin D-related disorders 4.) Renal failure

Question 40

Macrophages activate a vit. D precursor

Answer 40

Sarcoidosis

Question 40

Cause no clinical dysfunction, but on occasion massive involvement of the lungs produces remarkable x-ray images and respiratory compromise. Massive deposits in the kidney (nephrocalcinosis) may in time cause renal damage

Answer 40

Mineral salts