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MLS 222/L PRELIMS > CONT. LEC MOD 1 UNIT 2 > Flashcards

CONT. LEC MOD 1 UNIT 2 Flashcards

1
Q

the morphologic hallmark of irreversible injury and necrosis

A

nuclear changes

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2
Q

a nuclear change characterized by chromatin clumping and shrinking with increased basophilia

A

pyknosis

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3
Q

a nuclear change characterized by fragmentation of chromatin

A

karyorrhexis

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4
Q

a nuclear change characterized by fading of chromatin material and disappearance of stainable nuclei

A

karyolysis

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5
Q

necrotic cells are removed by

A

heterolysis by infiltrating leucocytes

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6
Q

A localized area of coagulative necrosis is called an

A

infarct

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7
Q

a pattern of necrosis which results in characteristic digestion, softening, and liquefaction of tissue.

A

liquefactive necrosis

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8
Q

ischemic injury to the CNS results in gangrenous necrosis. T or F

A

False. Liquefactive necrosis

After the death of CNS cells, liquefaction is caused by AUTOLYSIS

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9
Q

The necrotic material in liquefactive necrosis is caramel yellow because of the presence of pus. T or F

A

False. creamy gurl.

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10
Q

It is seen in focal bacterial or occasionally fungal infections that stimulate inflammation and in suppurative infections characterized by the formation of pus (liquefied tissue debris and neutrophils) by heterolytic mechanisms.

A

liquefactive necrosis

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11
Q

a pattern of necrosis which occurs as part of granulomatous inflammation and is a manifestation of partial immunity caused by the interaction of T lymphocytes (CD4+, CD8+, and CD4-CD8-), macrophages, and probably cytokines, such as interferon-γ, derived from these cells

A

caseous necrosis

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12
Q

Caseous necrosis combines features of both fibrinoid necrosis and liquefactive necrosis. T or F

A

False. coagulative necrosis and liquefactive necrosis

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13
Q

why is caseous necrosis named like this?

A

it has a cheese-like (caseous) consistency, a friable

white appearance on gross examination

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14
Q

caseous necrosis has an amorphous eosinophilic appearance on histologic examination. T or F

A

True

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15
Q

pneumonia is the leading cause of caseous necrosis. T or F

A

False tuberculosis

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16
Q

Gangrenous necrosis most often affects the lower extremities or bowel and is secondary to vascular occlusion (blockage of blood vessel). T or F

A

True

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17
Q

Not a specific pattern of cell death but is a commonly used term in clinical practice wherein it is usually applied to a limb, generally the lower leg that has lost is blood supply

A

gangrenous necrosis

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18
Q

When complicated by infective heterolysis and consequent liquefactive necrosis, gangrenous necrosis is called liquid gangrene. T or F

A

False wet gangrene

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19
Q

When characterized primarily by coagulative necrosis without liquefaction, gangrenous necrosis is called coagulated gangrene. T or F

A

False. dry gangrene

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20
Q

When infection is caused by Clostridium perfringens which produces gas and a feeling of crepitus it is called gas gangrene. T or F

A

True

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21
Q

A pattern of necrosis which is often associated with immune-mediated vascular damage.

A

Fibrinoid necrosis.
Occurs when complexes of antigens and antibodies are deposited in the walls of arteries. There is deposition of fibrin-like proteinaceous material in the arterial walls that appears to be smudgy and acidophilic.

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22
Q

2 forms of fat necrosis

A

traumatic fat necrosis

enzymatic fat necrosis

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23
Q

It occurs after a severe injury to tissue with high fat content, such as the
breast.

A

traumatic fat necrosis

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24
Q

a complication of acute hemorrhagic pancreatitis (a severe

inflammatory disorder of the pancreas)

A

enzymatic fat necrosis

  • involves proteolytic and lipolytic pancreatic enzymes diffuse into inflamed tissue and literally digest the parenchyma.
  • Fatty acids are then liberated by the digestion of fat and form calcium soaps (saponification, or soap formation). Vessels are eroded, with resultant hemorrhage.
  • Appear as grossly visible chalky- white areas which enable the surgeon or the pathologist to identify the lesion.
  • Histologic morphology: necrosis takes the form of shadowy outlines of necrotic fat cells with basophilic calcium deposits surrounded by inflammatory reaction
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25
Q

an orderly cell death which causes the cell to shrink and condense to disassemble its cytoskeleton and alter its cell surface so that phagocytic cells can attach to it and digest it rapidly before any leakage of its contents occurs, and neighboring cells usually remain healthy

A

apoptosis

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26
Q

apoptosis greek term for

A

falling away from

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27
Q

purpose of apoptosis

A
  • Eliminate cells that are no longer needed.

- Maintain a steady number of various cell populations in tissue

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28
Q

Progression is through a series of changes marked by a lack of inflammatory response include blebbing of plasma membrane, cytoplasmic shrinkage, and chromatin condensation

A

apoptosis

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29
Q

In apoptosis, there is also involution and shrinkage of affected cells and cell fragments, resulting in small round eosinophilic masses often containing chromatic remnants as exemplified by

A

councilman bodies in viral hepa

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30
Q

physiologic apoptosis

A
  • Destruction of cells during embryogenesis, implantation, organogenesis, developmental involution, and metamorphosis
  • Involution of hormone dependent tissues upon hormone withdrawal, such as endometrial cell breakdown during menstrual cycle, ovarian follicular atresia in menopause, regression of lactating breast after weaning, prostatic atrophy after castration.
  • Cell loss in proliferating cell populations, such as immature lymphocytes in the bone marrow and thymus and B lymphocytes in germinal centers that fail to express useful antigen receptors, and epithelial cells in intestinal crypts, so as to maintain a constant number (homeostasis)

-Elimination of potentially harmful self-reactive lymphocytes, either before or after they have completed their maturation, to prevent autoimmune
reactions.

-Death of host cells that have served their useful purpose, such as neutrophils in an acute inflammatory response and lymphocytes at the end of an immune response. In this case they are deprived of necessary survival signals, such as growth factors

31
Q

pathologic apoptosis

A

-DNA damage, Radiation, cytotoxic anticancer drugs and hypoxia can
damage DNA, either directly or by production of free radicals. If repair
mechanism cannot cope with the injury, the cell triggers intrinsic mechanisms that induce apoptosis. Elimination of the cell is a better alternative than risking malignant transformation.

-Accumulation of misfolded proteins, improperly folded proteins arise from
mutations in the genes encoding these proteins or because of extrinsic factors such as damage caused by free radicals. Excessive accumulation of these misfolded proteins in the ER is called ER STRESS, culminates in apoptotic cell death. Apoptosis caused by accumulation of misfolded proteins has been invoked as the basis of several degenerative diseases of the CNS and other organs.

-Cell death in certain infections, particularly viral infections, in which loss of
infected cells is largely due to apoptosis that may be induced by the virus
(adenovirus and HIV infections) or by the host immune response (as in viral
hepatitis). This is a T cell mediated response to viral proteins in an attempt to eliminate reservoirs of infection.

-Pathologic atrophy in parenchymal organs after duct obstruction, such as in the pancreas, parotid gland and the kidney

32
Q

Necrosis caused by accumulation of misfolded proteins has been
invoked as the basis of several degenerative diseases of the CNS and other organs. T or F

A

False. Apoptosis

33
Q

cells smaller, cytoplasm is denser and the organelles, although
relatively normal, are more tightly packed represents what morphology of apoptosis

A

cell shrinkage

34
Q

This is the most characteristic feature of apoptosis wherein chromatin aggregates peripherally under the nuclear membrane, into dense
masses of various shapes and sizes.

A

chromatin condensation

35
Q

Plasma membranes are thought to remain intact during necrosis until the last stages hence, do not spill their contents into extracellular environment
and usually do not trigger inflammation and keeps neighboring cells healthy. T or F

A

False. necrosis

36
Q

4 main pathways of abnormal intracellular accumulations

A
  • Inadequate removal of a normal substance secondary to defects in mechanisms of packaging and transport (fatty change)
  • Accumulation of an abnormal endogenous substance as a result of genetic or acquired defects in its folding, packaging, transport, or secretion (mutated forms of a1-antitrypsin)

-Faillure to degrade a metabolite due to inherited enzyme deficiencies
(storage diseases)

-Deposition and accumulation of an abnormal exogenous substance when the cell has neither the enzymatic machinery to degrade the substance nor the ability to transport it to other sites

37
Q

characterized by the accumulation of intracellular parenchymal triglycerides and is observed most frequently in the liver, heart, kidney

A

fatty change

38
Q

fatty change results from

A
  • decrease production of APOPROTEINS required for transport
  • overproduction fat cells
  • increased transport of triglycerides to affected cells
39
Q

Fatty change is thus linked to the disaggregation of ribosomes and consequent decreased protein synthesis caused by failure of ATP production in CCl4- injured cells. T or F

A

True

40
Q

used by cells to synthesize cell membranes

A

cholesterol

41
Q

The extracellular cholesterol may crystallize in the shape of long needles, producing quite distinctive clefts in tissue sections. T or F

A

False. cholesterol esters

42
Q

plaques, smooth muscle cells and macrophages within the
intimal layer of the aorta and large arteries are filled with lipid vacuoles, most of which are made up of cholesterol and cholesterol ester

A

atherosclerosis

43
Q

Intracellular accumulation of cholesterol within macrophages is also characteristic of acquired and hereditary hyperlipidemic states

A

xanthomas
-Clusters of foamy cells are found in the subepithelial connective tissue of the skin and in tendons, producing tumorous masses known as xanthomas.

44
Q

This refers to the focal accumulations of cholesterol-laden macrophages in
the lamina propria of the gallbladder.

A

cholesterolosis

45
Q

This lysosomal storage disease is caused by mutations affecting
an enzyme involved in cholesterol trafficking, resulting in cholesterol accumulation in multiple organs

A

niemann-pick disease, type C

46
Q

What are the Intermediate filaments, which provide a flexible intracellular scaffold that organizes the cytoplasm and resists forces applied to the cell,

A 
keratin filaments (characteristic of epithelial cells)
neurofilaments (neurons)
desmin filaments (muscle cells)
vimentin filaments (connective tissue cells)
glial filaments (astrocytes)
47
Q

The neurofibrillary tangle found in the brain in Alzheimer disease contains glial filaments. T or F

A

False. neurofilaments

48
Q

Certain forms of amyloidosis fall in this category of diseases. These disorders are sometimes called proteinopathies or protein-aggregation diseases

A

aggregation of abnormal proteins

49
Q

example of intracellular hyaline deposits

A

reabsorption droplets, russell bodies, alcoholic hyaline (composed of keratin intermediate filaments)

50
Q

Glycogen is found in renal tubular epithelial cells, as well as within liver cells, β cells of the islets of Langerhans, and heart muscle cells. T or F

A

True

51
Q

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

A

glycogen storage diseases, or glycogenoses.

52
Q

most common exogenous pigment

A

carbon (coal dust)

  • Accumulations of this pigment blacken the tissues of the lungs (anthracosis) and the involved. lymph nodes
  • In coal miners the aggregates of carbon dust may induce a fibroblastic reaction or even emphysema and thus cause a serious lung disease known as coal worker’s pneumoconiosis
53
Q

an insoluble pigment, also known as lipochrome or wear-and-tear pigment.

A

lipofuscin

54
Q

it is derived through lipid peroxidation of polyunsaturated lipids of subcellular membranes. Also, it is composed of polymers of lipids and phospholipids in complex with protein

A

lipofuscin

55
Q

its being a telltale sign of free radical injury and lipid peroxidation

A

lipofuscin

56
Q

fuscus (latin)

A

brown (brown lipid)

57
Q

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

A

lipofuscin

58
Q

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

A

lipofuscin

59
Q

This pigment is formed from tyrosine by the action of tyrosinase, synthesized in melanosomes of melanocytes within the epidermis

A

melanin

60
Q

Decreased melanin pigmentation is observed in albinism and vitiligo. T or F

A

True

61
Q

This pigment is a catabolic product of the heme moiety of hemoglobin and, to a minor extent, myoglobin.

A

bilirubin

62
Q

In various pathologic conditions, bilirubin accumulates and stains the blood, sclera, mucosae, and internal organs, producing a yellowish discoloration called

A

jaundice

63
Q

jaundice associated with destruction of red cells

A

hemolytic jaundice

64
Q

jaundice associated with parenchymal liver damage

A

hepatocellular jaundice

65
Q

jaundice associated with intra- or extrahepatic obstruction of the biliary
tract.

A

obstructive jaundice

66
Q

a hemoglobin-derived, golden yellow-to-brown, granular or crystalline pigment that serves as one of the major storage forms of iron

A

hemosiderin

67
Q

Iron is normally carried by specific transport protein

A

transferrins

68
Q

Ferritin is a constituent of most cell types. When there is a local or systemic excess of iron, ferritin does not form hemosiderin granules, which are easily seen with the light micro. T or F

A

False, they form hemosiderin granules

69
Q

Hemosiderin pigment represents aggregates of ferritin micelle. T or F

A

True

70
Q

The best example of localized hemosiderosis is

A

common bruise

71
Q

Local or systemic excesses of iron cause hemosiderin to accumulate within cell

A

True

72
Q

After removal of iron, the heme moiety is converted first to biliverdin (“red bile”) and then to bilirubin (“green bile”).

A

False. biliverdin = green bile

bilirubin = red bile

73
Q

the iron released from heme is incorporated into ferritin and eventually
hemosiderin.

A

True

74
Q

causes of hemosiderosis

A

-increased absorption of dietary iron
-hemolytic anemias, in which abnormal quantities of iron are released from
erythrocytes
-repeated blood transfusions because the transfused red cells constitute an exogenous load of iron

MLS 222/L PRELIMS (2 decks)

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