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MLS 222/L PRELIMS > LAB EXERCISE 1A > Flashcards

LAB EXERCISE 1A Flashcards

1
Q

Two main types of body cells

A

Epithelial and Mesenchymal Cells

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2
Q

Who first published cellular theory of disease?

A

Rudolf Virchow

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3
Q

A variety of stresses a cell encounters as as a result of changes in its internal and external environment.

A

Cell Injury

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4
Q

A result of persistent cell injury

A

Cell Death

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5
Q

A reversible cell injury has residual effects which include

A

Degenerations, Subcellular Alterations, and Intracellular Accumulations

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6
Q

These are reversible functional and structural responses to more severe physiologic stresses and some pathologic stimuli

A

Cellular Adaptations

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7
Q

A cellular adaptive response which is characterized by the increase in cell size and functional activity

A

Hypertrophy

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8
Q

It is characterized by a decrease in the size and metabolic activity of the cells

A

Atrophy

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9
Q

A change in the phenotype of cells

A

Metaplasia

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10
Q

Increase in the number of cells

A

Hyperplasia

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11
Q

Irreversible injury leads to

A

Cell Death

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12
Q

Metabolic derangement in cells and chronic injury may be associated with

A

Intracellular Accumulations (Proteins, Lipids, Carbohydrates)

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13
Q

Calcium deposition at sites of cell death causes

A

Pathologic Calcification

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14
Q

Cell death is also a normal and essential process in embryogenesis. T or F

A

True

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15
Q

Two principal pathways of cell death

A

Necrosis and Apoptosis

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16
Q

Apoptosis may be normal or pathological. T or F

A

True

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17
Q

Necrosis is may be normal or pathological. T or F

A

False

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18
Q

Injurious Stimulus: Chronic Irritation

A

Metaplasia

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19
Q

Injurious Stimulus: Increased demand, increased stimulation (by growth factors, hormones)

A

Hyperplasia, Hypertrophy

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20
Q

Injurious Stimulus: Decreased stimulation

A

Atrophy

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21
Q

This is due to cumulative sublethal injury over long life span

A

Cellular Aging

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22
Q

Most common stimulus for hypertrophy of muscle

A

Increased workload

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23
Q

Most common stimulus for hypertrophy of muscle

A

Increased workload

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24
Q

In hypertrophy, the increase in the size of the cells is due to

A

Synthesis of more structural components of the cells

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25
Q

Hypertrophy can be physiologic or pathologic. T or F

A

True

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26
Q

Most common pathologic hypertrophy due to increased workload

A

Hypertrophy of the Heart

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27
Q

Massive growth of uterus during pregnancy is an example of

A

Physiologic Hypertrophy

  • due to the stimulation caused by ESTROGENIC HORMONES acting on smooth muscle estrogen receptors
  • results in INCREASED synthesis of smooth muscle PROTEINS, hence the increase in cell size
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28
Q

Enlarged uterus cell morphology

A
  • Large plump cells

- The spindle shape of the muscle cells are no longer seen

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29
Q

Morphology of the pathologic hypertrophy of the myocardium

A
  • Enlarged Muscle Fibers

- Enlarged nuclei

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30
Q

Ultrastructural analysis of the pathologic hypertrophy of the myocardium

A
  • Increased synthesis of DNA and RNA
  • Increased protein synthesis
  • Increased number of organelles (mitochondria, ER, myofibrils)
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31
Q

Hyperplasia only takes place if the cell population is capable of dividing. T or F

A

True

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32
Q

This adaptive response typically occur as a result of hormonal stimulation

A

Hyperplasia

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33
Q

Histologic characteristic of Endometrial Hyperplasia

A
  • Increased glandular and stromal cells
  • grossly visible nodules
  • irregular crowding of epithelial cells lining the glands
  • cystic dilation
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34
Q

Histologic characteristic of Atrophic Brain

A

Narrow gyri (spaces between sulci) and widened sulci

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35
Q

Causes of Atrophy

A
  • Decrease workload
  • Loss of Innervation (Denervation Atrophy)
  • Diminished Blood Supply
  • Inadequate nutrition
  • Loss of endocrine stimulation
  • Pressure
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36
Q

A cellular adaptive response wherein one DIFFERENTIATED cell type is replaced by another cell type

A

Metaplasia

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37
Q

Columnar Cells of Bronchial Mucosa are changed in to _________ when irritated by cigarette smoke

A

Stratified Squamous Epithelium

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38
Q

Increased amounts of CSF as a compensatory mechanism for a person who has brain atrophy is a phenomenon termed as

A

Hydrocephalus ex vacuo

-body abhors empty space

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39
Q

What activities are lost when columnar cells are changed into stratified squamous epithelium

A

Mucus secretion and ciliary action

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40
Q

Common form of cancer in respiratory tract is composed of

A

squamous cells

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41
Q

The influences that predispose to metaplasia, if persistent, may initiate malignant transformation in metaplastic epithelium. T or F

A

True

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42
Q

Example of Metaplasia from SQUAMOUS to COLUMNAR

A

Barret Esophagus

  • esophageal squamous epithelium is replaced by intestinal-like columnar cells under the influence of REFLUXED GASTRIC ACID
  • usually cancer may arise in these areas
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43
Q

It is the formation of cartilage, bone, or adipose tissue (mesenchymal tissues) in tissues that normally do not contain these elements

A

Connective Tissue Metaplasia

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44
Q

An example of connective tissue metaplasia wherein bone forms in muscle after intramuscular hemorrhage

A

Myositis ossificans

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45
Q

Metaplasia cannot progress to dysplasia. T or F

A

False

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46
Q

Dysplasia may still be reversible if the stimulus is discontinued, but more often than not, it progresses to

A

Neoplasia

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47
Q

Cause of Cell Injury: Hypoxia (low oxygen levels in tissues) and anoxia (absence of oxygen)
Pathogenesis:
-Circulatory disturbances
-Inadequate oxygen intake

A

Myocardial Infarct Strangulation

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48
Q

Cause of Cell Injury: Toxin
Pathogenesis:
-Direct Toxicity
-Indirect Toxicity

A

Mercury Poisoning

Carbon Tetrachloride Poisoning

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49
Q 
Cause of Cell Injury: Microbes
Pathogenesis: 
-Bacterial exotoxins
-Direct (viral) cytopathic effect
-Indirect (immune-mediated cytotoxicity)
A
  • Food poisoning

- Viral infections

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50
Q

Cause of Cell Injury: Inflammation and immune
reactions
Pathogenesis: Action of cytokines and
complements

A

Autoimmune Disease

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51
Q

Cause of Cellular Injury: Genetic and metabolic disorders
Pathogenesis: Disruption of metabolic pathways
Abnormal metabolism

A
  • Lysosomal storage disease

- diabetes

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52
Q

Term (in conventional description) used to denote morphology of reversible cell injury

A

Degeneration

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53
Q

Morphologic form of reversible cell injury which is characterized by the accumulation of water within the cytoplasm

A

Hydropic Change

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54
Q

Synonym of hydropic change for gross appearance of the affected organ

A

Cloudy swelling

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55
Q

Vacuolar degeneration observed in “hydropic change” morphological form of reversible cell injury is due to

A

Cytoplasm Vacuolation

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56
Q

Mitochondrial swelling seen in hydropic change is due to

A

the water crossing the plasma membrane and entering the hyaloplasm (the clear, semi-fluid material between the meshes of the cell reticulum) and also accumulates within the mitochondria

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57
Q

How do membrane-bound vacuoles form in hydropic change

A

they from from the invaginations of the plasma membrane and ER

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58
Q

This is the most common and earliest form of cell injury from almost all causes

A

Hydropic Change

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59
Q

Hydropic change results from

A

Impaired regulation of sodium and potassium at the cell membrane
resulting in
-INTRACELLULAR ACCUMULATION of SODIUM
-ESCAPE of POTASSIUM

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60
Q

Intracellular accumulation in hydropic change leads to

A
  • rapid flow of water into the cell to MAINTAIN ISO-OSMOTIC conditions
  • this leads to cellular swelling and INFLUX of CALCIUM
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61
Q

Gross Morphologic Features of Hydropic Change

A

-The affected organ such as kidney, liver, pancreas, or heart
muscle is ENLARGED due to SWELLING
-The cut surface BULGES OUTWARDS
-slightly OPAQUE

62
Q

Microscopic Morphologic Feature of Hydropic Change

A
  • swollen cells
  • compressed microvasculature
  • small clear vacuoles seen in the cells (vacuolar degeneration), represent distended cisternae of the ER
  • Cytoplasmic blebs
  • Nucleus may appear pale
63
Q

Renal Tubular Epithelial Cell damaged by hypoxia is characterized by

A
  • swollen mitochondria

- vacuoles in mitochondria pushed the cristae apart

64
Q

Summary of consequences of hydropic change in cells

A
  • swollen microvilli due to influx of water in cytoplasm
  • Invagination of the cell membrane gives rise to fluid-filled vacuoles
  • swollen mitochondria (part of vacuolar degeneration)
  • dilated RER (part of vacuolar degeneration)
  • swollen cells lose contact with adjacent cells at the site of cell-to-cell junctions (desmosomes)
65
Q

The earliest light microscopic evidence of cellular injury

A

loss of normal staining intensity

66
Q

Normal cytoplasm stained with H&E have light pink with a faint tint of blue. Why is there a faint tint of blue?

A

due to ribosomal RNA

67
Q

What happens when there is sub-lethal cellular damage

A
  • ribosomes are reduced in number

- the normal blue cytoplasmic tint is lost

68
Q

Hyaline means

A

Hyalos: glass

69
Q

It is a descriptive histologic term for glassy, homogenous, eosinophilic appearance of material

A

Hyaline

70
Q

Hyaline change is not in any way related to heterogenous pathologic conditions. T or F

A

False

71
Q

Hyaline change may be intracellular or extracellular. T or F

A

True

72
Q

Fibrin and amyloid have hyaline appearance. T or F

A

True

73
Q

Intracellular Hyaline is mainly seen in

A

epithelial cells

74
Q

Hyaline droplets is due to

A

excessive reabsorption of plasma proteins

75
Q

Zenker’s degeneration is due to

A

Hyaline degeneration of rectus abdominal muscle

76
Q

Zenker’s degeneration is characterized by

A

the loss of muscle fibrillar staining and the muscle becomes glassy and hyaline

77
Q

Zenker’s degeneration is occurring in

A

typhoid fever

78
Q

It is represented by aggregates of intermediate filaments in the hepatocytes in alcoholic liver cell injury

A

Mallory’s hyaline

79
Q

Type of hyaline inclusions seen in viral infection

A

Nuclear or cytoplasmic hyaline inclusions

80
Q

Russell’s bodies are the

A

excessive immunoglobulins in the RER of plasma cells

81
Q

Extracellular hyaline (more difficult to analyze) is seen in

A

connective tissues

82
Q

Examples of Extracellular Hyaline

A
  • hyaline degeneration in leiomyomas of the uterus
  • hyalinised old scar of fibrocollagenous tissues
  • hyaline arteriosclerosis in renal vessel (hypertension, diabetes mellitus)
  • hyalinised glomeruli in chronic glomerulonephritis
  • corpora amylacea
83
Q

It is an example of extracellular hyaline which is characterized by rounded masses of concentric hyaline laminae seen in the prostate (elderly), brain and spinal cord in old age, and in old infarcts of the lung.

A

corpora amylacea

84
Q

mucus is a combination of

A

proteins complexed with mucopolysaccharides

85
Q

what is the chief constituent of mucus?

A

mucin (a glycoprotein)

86
Q

connective tissue mucin is termed as

A

myxoid (mucus like)

87
Q

mucin is normally produced by

A

epithelial cells of the mucous membranes and mucous glands

88
Q

both types of mucin (produced by epithelial cells and in connective tissue) are stained by

A

alcian blue

89
Q

Epithelial mucin stains negatively with periodic acid-Schiff (PAS) while connective tissue mucin is PAS positive. T or F

A

False. it’s the other way around.

Note: connective tissue mucin stain POSITIVELY with COLLOIDAL IRON

90
Q

Example of mucoid change associated with epithelial mucin

A
  • catarrhal inflammation of mucous membrane (respiratory, alimentary, uterus)
  • obstruction of duct leading to mucocele in the oral cavity and gall bladder
  • cystic fibrosis of pancreas
  • mucin-secreting tumors (ovary, stomach, large bowel)
91
Q

What are the subcellular alterations occurring during cell injury

A
  • cytoskeletal changes
  • lysosomal changes
  • SER changes
  • mitochondrial changes
92
Q

example of mucoid change associated with connective tissue mucin

A

-Mucoid or myxoid degeneration in some tumors
(myxomas, neurofibromas, fibroadenoma, soft tissue
sarcomas, etc)
-Dissecting aneurysm of the aorta due to Erdheim’s
medial degeneration and Marfan’s syndrome.
-Myxomatous change in the dermis in myxoedema.
-Myxoid change in the synovium in ganglion on the
wrist

93
Q

a subcellular alteration characterized by the following:

  • Defective microtubules
  • Defective microfilaments
  • Accumulation of intermediate filaments
A

cytoskeletal changes

94
Q

a subcellular alteration characterized by the following:

  • Heterophagy
  • Autophagy
  • Indigestible materials
  • Storage diseases
A

lysosomal changes

95
Q

a subcellular alteration characterized by the following:
Megamitochondria
-Alterations in the number of mitochondria
-Oncocytoma
-Myopathies

A

mitochondrial changes

96
Q

what are the two categories of intracellular accumulation

A
  • normal cellular constituent (water, lipids, proteins, carbohydrates)
  • abnormal substance (exogenous, endogenous)
97
Q

these are intracellular accumulations under abnormal substance like mineral or products of infectious agents

A

exogenous

98
Q

these are products of abnormal synthesis or metabolism, what type of intracellular accumulations are these?

A

abnormal substance: endogenous

99
Q

intracellular accumulations may be located in

A

cytoplasm (frequently with phagosomes)

nucleus

100
Q

in some cases, intracellular accumulations may be from the cell’s production of abnormal substance, and in others it may be just storing products of pathologic processes occurring elsewhere in the
body. T or F

A

False

101
Q

what are the 3 groups of abnormal intracellular accumulations

A
  • Accumulation of constituents of normal cell metabolism produced in excess (accumulation of lipids, proteins and carbohydrates)
  • Accumulation of abnormal substances produced as a result of abnormal metabolism due to lack of some enzymes.
  • Accumulation of pigments e.g. endogenous pigments under special circumstances, and exogenous pigments due to lack of enzymatic mechanisms to degrade the substances or transport them to other sites
102
Q

Accumulation of lipids in the liver is an example of

A

intracellular accumulation of intermediate metabolites

103
Q

fat accumulation in the liver, also known as

A

steatosis

104
Q

fat is stored in the liver in what form

A

triglycerides

105
Q

steatosis or fatty change represents the

A

intracytoplasmic accumulation of triglyceride (neutral fats) of parenchymal organs like liver, myocardium and kidney

106
Q

major organ involved in fat metabolism

A

liver

107
Q

what are the causes of steatosis

A
  • toxins
  • protein malnutrition
  • diabetes mellitus
  • obesity
  • anoxia (“Halla sino yon?” “Di mo kilala? Anoxia ni marites” eheheh)
108
Q

excess accumulation of triglycerides results in

A

defective metabolism and export of lipids

109
Q

gross morphology of fatty change

A
  • enlarged liver
  • has tense glistening capsule and rounded margins
  • pale-yellow to yellow
  • greasy to touch
110
Q

microscopic morphology of fatty change

A
  • presence of numerous lipid vacuoles in the cytoplasm of hepatocytes
  • The vacuoles are initially small and are present around the nucleus (microvesicular)
  • But with progression of the process, the vacuoles become larger pushing the nucleus to the periphery of the cells (macrovesicular).
  • At times, the hepatocytes laden with large lipid vacuoles may rupture and lipid vacuoles coalesce to form fatty cysts.
  • Infrequently, lipogranulomas may appear consisting of collections of lymphocytes, macrophages, and some multinucleate giant cells.
  • Fat can be demonstrated in fresh unfixed tissue by frozen section followed by fat stain such as Sudan dyes (Sudan III, IV, Sudan black) and oil red O. Alternatively, cosmic acid which is a fixative as well as a stain can be used to demonstrate fat in tissue
111
Q

These intracellular accumulations appear as rounded, eosinophilic droplets, vacuoles, or aggregates in the cytoplasm

A

proteins

112
Q

through electron microscopy, intracellular accumulation of proteins can be

A
  • amorphous
  • fibrillar
  • crystalline
113
Q

This is a disorder characterized by the deposit of abnormal proteins in extracellular spaces

A

amyloidosis

114
Q

protein loss in the urine

A

proteinuria

115
Q

Intracellular Accumulation of Proteins can be due to

A
  • Reabsorption droplets in proximal renal tubules
  • Proteins that accumulate may be normal secreted proteins
  • Defective intracellular transport and secretion of critical proteins
  • Accumulation of cytoskeletal proteins.
  • Aggregation of abnormal proteins.
116
Q

This is a readily available energy source stored in the cytoplasm of healthy cells. They also appear as clear vacuoles within the cytoplasm.

A

glycogen

117
Q

a group of related genetic disorders where glycogen accumulates
within the cells

A

Glycogenoses or glycogen storage diseases

118
Q

In this disease, glycogen is found in renal tubular epithelial cells, as well as within liver cells, Beta cells of the islets of Langerhans, and heart muscles.

A

Diabetes Mellitus

119
Q

This is a fibrillar proteinaceous substance with common morphological appearance, staining properties and physical structure but with variable protein (or biochemical) composition.

A

Amyloid

120
Q

An organ containing amyloid stains

A

brown - iodine

violet - addition of dilute sulfuric acid

121
Q

By H&E staining under light microscopy, amyloid appears as extracellular, homogenous, structureless and eosinophilic hyaline material. T or F

A

True

122
Q

amyloid stains positive with Congo red staining and shows apple-green birefringence on polarizing microscopy. T or F

A

True

123
Q

the term used for a group of diseases characterized by the extracellular deposition of amyloid.

A

Amyloidosis

124
Q

staining Characteristics of Amyloid

A

Stain - Appearance

H&E - Pink, hyaline, homogenous

Methyl violet/crystal violet - Metachromasia: rose-pink

Congo red - Light microscopy: pink-red
Polarizing light: red-green bifringence

Thioflavin-T/Thioflavin-S - Ultraviolet light: fluorescence

Immunohistochemistry (antibody against fibril protein) - Immunoreactivity: Positive

Non-specific stains:
•Standard toluidine blue - Orthochromatic blue, polarizing ME dark red
• Alcian blue - Blue-green
• PAS - pink

125
Q

Classification of Amyloidosis and Organs Commonly Involved

A

A. Systemic (Generalized) Amyloidosis

CATEGORY - ORGANS

Primary - Heart, bowel, skin, nerves, kidney

Secondary (Reactive) - Liver, spleen, kidneys, adrenals

Hemodialysis-associated - Synovium, joints, tendon sheaths

B. Localized Amyloidosis

CATEGORY - ORGANS

Senile cardiac - heart

senile cerebral - Cerebral vessels, plaques, neurofibrillary tangles

endocrine - Thyroid, Islets of Langerhans

tumour-forming - respective anatomic location

126
Q

Gross morphologic feature of amyloidosis

A
  • affected organ is enlarged
  • pale
  • rubbery
  • cut surface shows firm, waxy, and transparent parenchyma which takes positive staining with the iodine test
127
Q

microscopic morphologic feature of amyloidosis

A
  • deposits of amyloid are found in the extracellular locations
  • initially in the walls of small blood vessels producing microscopic changes and effects
  • later the deposits are in large amounts causing macroscopic changes and effect of pressure atrophy
128
Q

2 patterns of the amyloidosis of the spleen

A
  • sago spleen

- lardaceous spleen

129
Q

this is one of the patterns of amyloidosis of the spleen wherein gross observation includes the translucent and pale and waxy nodules resembling sago grains.

microscopic observation includes amyloid deposits that begin in the walls of the arterioles of the white pulp and ay subsequently replace the follicles

A

sago spleen

130
Q

In this pattern of amyloidosis of the spleen, gross appearance is marked bysplenomegaly and cut surface of the spleen shows map-like areas on amyloid

microscopically: the deposits involve the walls of splenic sinuses and the small arteries and in the connective tissue of the red pulp

A

lardaceous spleen

131
Q

Grossly, the liver is often enlarged, pale, waxy and firm. Histologically, the
features are seen.

-The amyloid initially appears in the space
of Disse (the space between the hepatocytes and sinusoidal endothelial
cells)
-Later, as the deposits increases, they compress the cords of hepatocytes so that eventually the liver cells are shrunken and atrophic and replaced by amyloid. However, hepatic function remains normal even at an advanced stage of the disease

A

Amyloidosis of the liver

132
Q

These are colored substances, some of which are
normal constituents of cells (melanin), or abnormal
constituents that accumulate in cells under special
circumstances

A

Pigments

133
Q

In cell death, what are the 3 forms of nuclear changes

A

-pyknosis m a r k e d b y
condensation of the chromatin
(pylons means “dense” in Greek)

-karyorrhexia characterized by
f r a g m e n t a t i o n i n t o s m a l l e r
particles, colloquially called,
nuclear dust

-karyolysis which involves dissolution of nuclear structure and lysis of chromatin by enzymes,
like DNase and RNase

134
Q

The morphologic appearance of necrosis is due to

A

denaturation of intracellular proteins

and enzymatic digestion of the lethally injured cell.

135
Q

Necrotic cells are unable to maintain membrane integrity and their contents often leak out, which can elicit inflammation in the surrounding tissue. T or F

A

True

136
Q

where do the enzymes that digest necrotic cells originate

A

derived from the lysosomes of the dying cells themselves and from the lysosomes of leukocytes that are called in as part of the inflammatory reaction

137
Q

Necrotic cells show increased eosinophilia in H&E stains. T or F

A

True. due in part to the loss of cytoplasmic RNA that
binds the blue dye, hematoxylin, and in part to
denatured cytoplasmic proteins that bind the red dye,
eosin. The necrotic cell may have a more glassy
homogeneous appearance than do normal cells, as a
result of the loss of glycogen particles

138
Q

Dead cells may be replaced by

A 
myelin figures ( derived from damaged cell 
membranes)
139
Q

Type of Necrosis: coagulative necrosis

A

Occurs due to an infarct (lack of blood from from an obstruction causing ischemia) and can occur in all the cells of the body except the brain. Cells that undergo coagulative necrosis can become dry, hard, and white. Gel-like appearance occurs in dead tissues but the architecture of the cells is maintained for at least some days. Coagulation occurs as the proteins are degraded and denatured, and an opaque film starts to form.

Gross appearance (A): A pale segment may be seen in contrast to surrounding healthy tissues. The segment may be hard to touch.
Microscopic appearance (B), In an H&E staining tissue, eosinophilia like cell (cells presenting pink on a histology slide) will be noticeable. Anucleated cells should by observable with preserved cell outlines. Compare the appearance of (I) to the normal part of the kidney (N)
140
Q

Type of Necrosis: Liquefactive necrosis

A

Associated from bacterial, viral, parasites or fungal infections. Unlike coagulative necrosis, liquefactive necrosis from a viscous liquid mass as the dead cells are being digested. Microorganisms release enzymes to degrade cells and initiate an immune and inflammatory response. Cellular dissolution and digestion of dying cells may also release further enzymes speeding up the liquefying process. Microbes stimulate the accumulation of leukocytes and is called pus.

Gross appearance (A): Liquid-like layer can be seen; pus should be present. Yellowing, softening or swelling of thetissue should be seen. Malacia (softening, or loss of consistency) should be present. A cystic space should be present for tissue 
resolution.

Microscopic appearance (B): Macrophages and neutrophils, both dead and alive, should be present. Debris and lysed cells should be seen with inflammation. Partial space should be filled with lipids and debris. There is a loss of neurons and glial cells, with the formation of clear space

141
Q

Type of necrosis: Gangrenous necrosis

A

This does not demonstrate a specific pattern of cell death but is used in clinical practice to describe the condition. Gangrenous necrosis generally describes the damage that has occurred to the extremities (especially lower) where there is severe ischemia. These extremities lack in blood supply and oxygen and typically cause coagulative necrosis at different tissue planes (dry gangrene). If bacterial infection occurred, liquefactive necrosis could also be occurring due to the degrading enzymes and the involvement of leukocytes resulting to wet gangrene.

Gross appearance: Black skin is generally seen with a degree of putrefaction (process of decay or rotting in a body or other organic matter). The tissue may look ‘mummified.’

Microscopic appearance (A): Due to the ischemia that would suggest dry gangrene, coagulative necrosis histological traits should be seen. If there is bacterial infection which would suggest wet gangrene, liquefactive necrosis histological traits should be seen.

142
Q

type of necrosis: caseous necrosis

A

Occurs when the immune system and body cannot successfully remove the foreign noxious stimuli. For example. tuberculosis is a prime example where there in an aberrant immune response (alveolar macrophages are not responding correctly) to the bacteria as the bacteria has infected the macrophages. The immune system seals off the foreign matter by using fibroblasts and white blood cells such as lymphocytes, neutrophils, NK cells, dendritic cells and macrophages. A granuloma may form with fibroblast cells (creates an encasing layer), leukocytes and the formation of Langhans giant cells (fusion of epithelia cells). The organism is not killed but contained.

Gross appearance (A): A yellow-white soft cheesy sphere that is enclosed by a distinct border.

Microscopic appearance (B): A granuloma should be present. The core is necrotic and uniformly eosinophilic, which is surrounded by a border of activated macrophages and lymphocytes. The core is structureless and should have debris and lysed cels. Langhans giant cells may be seen, and inflammation should also be noticed and present. There is a fibrous case surrounding and enclosing the core; hence fibroblasts should also be seen

143
Q

type of necrosis: fat necrosis

A

This is used to describe the destruction of fat due to pancreatic lipase that have been released into the surrounding tissues. The pancreas itself is at risk along with the peritoneal cavity. Acute pancreatitis causes the pancreatic enzymes to leak out from the acinar cells. Once the enzymes come into contact with fat cells, their plasma membrane is liquefied, releasing the fats/triglycerides. The fatty acids combine with calcium through a process called saponification. An insoluble salt is created and
gives the appearance of a chalky-white area. Infections, viruses, trauma, ischemia and toxins could be responsible for the pancreas to be damaged and release its enzymes. Breast tissues can also have fat necrosis to which is triggered from trauma.

Gross appearance (A): Soft chalky-white area should be seen on the pancreas.

Microscopic appearance (B): Basophilic (bluish) calcium deposits are present. Anucleated adipocytes with a cytoplasm that is more pink and contains amorphous mass of necrotic material. Inflammation would be present

144
Q

Type of necrosis: fibrinoid necrosis

A

This is associated with vascular damage (cause mainly by autoimmunity, immune complex deposition, infections) and the exudation of plasma proteins (such as fibrin). This pattern typically occurs due to a type 3 hypersensitivity, where an immune complex is formed between an antigen (Ag) with an antibody (Ab). The Ag-Ab complex may be deposited in the vascular walls causing inflammation, complement being activated, and phagocytic cells are recruited, which could be releasing oxidants and other enzymes causing further damage and inflammation.Fibrin, a non-globular protein involved in clotting of blood, is leaked out of the
vessels. The results create an amorphous appearance that is bright pink in an H&E stain. This is called ‘fibrinoid’ appearance, which means fibrin-like.

Gross appearance: Usually not grossly discernible

Microscopic appearance: An amorphous appearance that is bright pink in an H&E stain. The deposition of fibrinoid are surrounding the blood vessels. Inflammation should be present.

145
Q

programmed cell death

A

apoptosis

146
Q

active form of cell death

A

apoptosis, because it is energy dependent and requires activation of
a specific set of genes and enzymes

147
Q

what are the genes being activated in apoptosis

A

suicide genes

148
Q

morphologic changes in apoptosis

A
  • Cell shrinkage: The cell is smaller in size; the cytoplasm is dense (Figure 1a-22A); and the organelles, though relatively normal, are more tightly packed. (Recall that in other forms of cell injury, an early feature is cell swelling, not shrinkage.)
  • Chromatin condensation: This is the most characteristic feature of apoptosis. The chromatin aggregates peripherally, under the nuclear membrane, into dense masses of various shapes and sizes (Figure 1a-22B). The nucleus itself may break up, producing two or more fragments.
  • Formation of cytoplasmic blebs and apoptotic bodies: The apoptotic cell first shows extensive surface blebbing, then undergoes fragmentation into membrane-bound apoptotic bodies composed of cytoplasm and tightly packed organelles, with or without nuclear fragments (Figure 1a-22C).
  • Phagocytosis of apoptotic cells or cell bodies, usually by macrophages: The apoptotic bodies are rapidly ingested by phagocytes and degraded by the phagocyte’s lysosomal enzymes.
149
Q

the necrotic cell appears as a round or oval mall (? baka ball?) of intensely eosinophilic cytoplasm with fragments of dense nuclear chromatin in tissue stains with H&E. T or F

A

False. apoptotic cell

150
Q

Apoptosis elicit inflammation. T or F

A

False. hence, it is more difficult to detect histologically. Also, the cell shrinkage and formation of apoptotic bodies are rapid and the pieces are quickly phagocytosed, considerable apoptosis may occur in
tissues before it becomes apparent in histologic sections.

MLS 222/L PRELIMS (2 decks)

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