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Histopathologic and Cytologic Techniques > LEC Module 1: Unit 1-2 > Flashcards

LEC Module 1: Unit 1-2 Flashcards

1
Q

study of the structural, biochemical, and functional changes in cells, tissues, and organs that underlie diseas

A

pathology

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2
Q

2 Traditional Divisions of Pathology

A

General Pathology

Systemic Pathology

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3
Q

division of pathology concerned with common reactions of cells and tissue to injurious stimuli
not tissue specific

A

General Pathology

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4
Q

division of pathology that examines the alterations and underlying mechanisms in organ specific diseases

A

Systemic pathology

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5
Q

4 aspects of disease process that form the core of pathology:

A
  1. etiology
  2. pathogenesis
  3. morphologic changes
  4. clinical manifestations
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6
Q

refers to the cause of disease

A

etiology

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7
Q

two general kinds of etiology

A

genetic and acquired

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8
Q

etiology that includes inherited mutations, and disease associated gene variants, or polymorphisms

A

genetic

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9
Q

refers to the sequence of biochemical and molecular events that follow the exposure of cells or tissues to injurious agent

A

pathogenesis

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10
Q

Structural alterations induced in the cells and organs of the body that are either characteristic or diagnostic of an etiologic process.

A

morphologic changes

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11
Q

pathology that traditionally uses morphologic changes to determine the nature of a disease and to follow its progression

A

diagnostic pathology

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12
Q

refers to the functional consequences of the disease

A

clinical manifestations

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13
Q

clinical manifestation that is objective and can be identified by another person (e.g. 39°C body temperature)

A

sign

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14
Q

clinical manifestation that is subjective and cannot be identified by anyone else.

A

symptoms

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15
Q

refers to the pathophysiological response to internal and external factors

A

disease

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16
Q

refers to a disruption of the disease to the normal or regular functions in the body or a part of the body

A

disorder

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17
Q

Refers to a disease or a disorder that has more than one identifying feature or symptom.

A

syndrome

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18
Q

refers to the determination of the nature of a disease expressed in a concise manner

A

diagnosis

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19
Q

refers to the forecast of the probable course and outcome of a disease, especially of the chances of recovery and estimate of severity

A

prognosis

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20
Q

disease that has a sudden onset or rapid course (less than a month)

A

acute

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21
Q

disease that has a slow onset or a long duration

A

chronic

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22
Q

Acute or chronic?

UPPER REPIRATORY TRACT INFECTION

A

acute

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23
Q

Acute or chronic?

APPENDICITIS

A

acute

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24
Q

Acute or chronic?

ASTHMA

A

Chronic

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25
Q

Acute or chronic?

BRONCHITIS

A

acute

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26
Q

Acute or chronic?

COPD

A

chronic

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27
Q

a disease with no identifiable cause or have limited literature describing the methodology to define it and has no clear diagnostic criteria.

A

idiopathic

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28
Q

pathology caused by a physician and their treatment (retained forceps after surgery)

A

iatrogenic

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29
Q

infection acquired outside a health care facility.

A

Community acquired infection

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30
Q

refers to hospital acquired infections

A

nosocomial

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31
Q

nosocomial infections should occur within __________ of hospital admission, _________ of discharge or ________ 30 days of operation

A

48 hours, 3 days, 30 days

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32
Q

Diseases that are not transmitted through contact with an infected or afflicted person.

A

Non communicable diseases (NCD)

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33
Q

4 main types of NCDs

A
  1. Cancer
  2. Cardiovascular diseases
  3. Chronic Respiratory diseases (Asthma and COPD)
  4. Diabetes
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34
Q

diseases that can be spread from one organism to another, including spread from one person to person or animal to humans

A

communicable diseases

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35
Q

animal to person transmission

A

zoonotic

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36
Q

to affect of contaminated someone with pathogenic microorganisms.

A

infectious

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37
Q

refers to spread of disease through direct bodily contact with an infected person, their discharges or an object or surface they have contaminated.

A

contagious

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38
Q

TRUE OR FALSE?

All communicable diseases are infectious.

A

True

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39
Q

TRUE OR FALSE?

All infectious disease are contagious.

A

FALSE

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40
Q

TRUE OR FALSE?

All contagious diseases are infectious.

A

TRUE

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41
Q

reversible functional and structural responses to changes in physiologic states and some pathologic stimuli, during which new but altered steady states are achieved, allowing the cell to survive and to continue its function

A

cell adaptation

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42
Q

4 forms of adaptation in response to environmental stress

A
  1. hypertrophy
  2. hyperplasia
  3. atrophy
  4. metaplasia
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43
Q

refers to an increase in the size of the cells resulting into an overall increase of the organ as well

A

hypertrophy

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44
Q

refers to hypertrophy that is due to increase in functional demand or by stimulation by hormones or growth factors

A

physiologic hypertrophy

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45
Q

refers to an increase in the size of an organ or tissue caused by an increase in number of cells in response to a stimulus.

A

hyperplasia

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46
Q

refers to the decrease in the size of an organ or tissue which results from a decrease in the mass of pre-existing cells.

A

atrophy

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47
Q

5 common causal factors of atrophy

A
  1. disuse
  2. nutritional or oxygen deprivation
  3. diminshed endocrine stimulation
  4. aging
  5. denervation
  6. pressure
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48
Q

intracytoplasmic vacuoles containing debris from degraded organelles which is a characteristic feature of atrophy

A

autophagic granules

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49
Q

refers to the replacement of one differentiated tissue by another

A

metaplasia

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50
Q

metaplasia that replaces columnar epithelium when bronchi, cervix, endometrium, or pancreatic duct are chronically irritated

A

squamous metaplasia

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51
Q

metaplasia which involves formation of new bone at sites of tissue injury

A

osseous metaplasia

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52
Q

metaplasia involving proliferation of hematopoietic tissue at sites other than the bone marrow, such as the liver and spleen

A

myeloid metaplasia

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53
Q

occurs when the limits of adaptive responses are exceeded and cells are exposed to injurious agents or stress, deprived of essential nutrients.

A

cell injury

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54
Q

Cell injury is ___________ up to a point, but if the injurious stimulus is persistent or
severe, the cell suffers ___________ injury and cell death may ensue.

A

reversible, irreversible

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55
Q

Determine the cellular response given the injurious stimulus:
increased demand or increased stimulation (growth factors & hormones)

A

hyperplasia, hypertrophy

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56
Q

Determine the cellular response given the injurious stimulus:
decreased nutrients or decreased stimulation

A

atrophy

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57
Q

Determine the cellular response given the injurious stimulus:
chronic chemical or physical irritation

A

metaplasia

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58
Q

Determine the cellular response given the injurious stimulus:
acute or transient cell injury

A

reversible injury

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59
Q

Determine the cellular response given the injurious stimulus:
progressive and severe cell injury including DNA damage

A

irreversible injury + cell death

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60
Q

6 causes of cell injury

A
  1. hypoxic cell injury
  2. free radical injury
  3. chemical cell injury
  4. infectious agents
  5. immune sytem
  6. genetic abnormalities
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61
Q

Oxygen deprivation or hypoxia causes cell injury by reducing ________

A

aerobic oxidative respiration

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62
Q

3 causes of hypoxia include:

A
  1. reduced blood flow (ischemia)
  2. inadequate oxygenation of the blood due to cardiorespiratory failure
  3. decreased oxygen-carrying capacity of the blood (anemia or carbon monoxide poisoning)
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63
Q

the first cell organelle affected by hypoxic cell injury

A

mitochondria

64
Q

during a hyposic cell injury, mitochondria undergoes decreased ________ and _________

A

oxidative phosphorylation and ATP synthesis

65
Q

4 events of early stage hypoxic cell ijury

A
  1. mitochondria affected
  2. intracellular swelling (due to decreased ATP causing failure of pump)
  3. ribosome disaggregation
  4. acidification and clumping nuclear chromatin
66
Q

2 morphologic signs of reversible hypoxic injury

A
  1. formation of myelin figures (whorl like structures from damaged membrane)
  2. cell blebs (surface deformity due to cytoskeleton disfunction)
67
Q

3 morphologic signs of irreversible hypoxic cell injury

A
  1. irrevesible damage to cell membrane leading to massive calcium influx
  2. calcification of mitochondria
  3. release of intracellular enzymes into the circulation (due to loss of membrane integrity)
68
Q

hypoxic injury becomes irreversible in neurons after ___________

A

3-5 minutes

69
Q

hypoxic cell injury becomes irreversible to myocardial cells and hepatocytes after ___________

A

1-2 hours

70
Q

hypoxic cell injury becomes irreversible to skeleltal muscle cells after ___________

A

many hours

71
Q

injury caused by molecules that have a single unpaired electron in the outer orbital

A

free radical injury

72
Q

examples of free radicals

A
  1. superoxide

2. hydroxyl radicals

73
Q

three mechanisms that degrade free radicals

A
  1. intracellular enzymes
  2. exogenous and endogenous antioxidants
  3. spontaneous decay
74
Q

two contrasting morphologic patterns of cell death

A
  1. necrosis

2. apoptosis

75
Q

it is the sum of the degradative and inflammatory reactions occurring after tissue death caused by injury

A

necrosis

76
Q

The causes of necrotic morphology are:

A
  1. denaturation of intracellular proteins

2. enzymatic digestion of lethally injured cells

77
Q

2 enzymatic processes that digest the necrotic cell

A
  1. autolysis

2. heterolysis

78
Q

refers to degradative reactions in cells caused by intracellular enzymes from lysozomes indigenous to the cell

A

autolysis

79
Q

occurs after the death of the organism and is not considered necrosis

A

postmortem autolysis

80
Q

It refers to cellular degradation by enzymes derived from sources extrinsic to the cell like leucocytes or macrophages

A

heterolysis

81
Q

necrosis, due to leaking content from inability to maintain membrane integrity, causes ________

A

inflammation

82
Q

The earliest histologic evidence of myocardial necrosis does not become apparent until

A

4-12 hours

83
Q

When large numbers of cells die the tissue or organ is said to be

A

necrotic

84
Q

Necrosis that results most often from a sudden cutoff of blood supply to an organ (ischemia), particularly the heart and kidney (solid organs).

A

coagulative necrosis

85
Q

The eosinophilic anucleate appearance of the cell due to intense intracellular acidosis denaturing structural proteins and releasing proteolytic enzymes from the lysosome

“

A

Tombstone appearanceof the cells.

86
Q

3 nuclear changes which are the morphologic of irreversible cell injury and necrosis

A
  1. Pyknosis
  2. Karyorrhesis
  3. Karyolysis
87
Q

Nuclear change where chromatin clumps and shrinks with increased basophilia

A

pyknosis

88
Q

Nuclear change involving fragmentation of chromatin

A

karyorrhexis

89
Q

Nuclear change involving fading of chromatin material and disappearance of stainable nuclei

A

karyolysis

90
Q

Necrotic cells in coagulative necrosis are removed by

A

heterolysis of leukocytes

91
Q

A localized area of coagulative necrosis is called

A

infarct

92
Q

Necrosis that results to characteristic digestion, softening, and liquefaction of tissue.

A

Liquefactive necrosis

93
Q

Liquefaction is caused by

A

autolysis

94
Q

examples of liquefactive necrosis

A
  1. ischemic injury to CNS
  2. focal bacteria
  3. fungal infections
95
Q

creamy yellow necrotic material made of liquefied tissue debris and neutrophils

A

pus

96
Q

mechanisms that generate free radicals

A

a. Normal metabolism
b. Oxygen toxicity
c. Ionizing radiation
d. Ultraviolet light
e. Drugs and chemicals
f. Reperfusion after ischemic injury

97
Q

mechanisms that generate free radicals

A

a. Normal metabolism
b. Oxygen toxicity
c. Ionizing radiation
d. Ultraviolet light
e. Drugs and chemicals
f. Reperfusion after ischemic injur

98
Q

What happens to normal cells when put under stress?

A

adaptation

99
Q

If the cell was unable to adapt in response to stress or injurious stimulus, what happens?

A

cell injury

100
Q

Refers to cell injury that is mild or transient

A

reversible injury

101
Q

Refers to cell injury that is mild or transient

A

reversible injury

102
Q

Refers to cell injury that is severe or progressive

A

irreversible cell injury

103
Q

Identify what cell adaptation is being exhibited:

Increase workload among body builders

A

physiologic hypertrophy

104
Q

Identify what cell adaptation is being exhibited:

estrogenic hormone induced increase in the uterine size during pregnancy

A

Physiologic hypertrophy

105
Q

Identify what cell adaptation is being exhibited:

Hemodynamic overload due to hypertension of faulty valves

A

Pathologic hypertrophy

106
Q

Identify what cell adaptation is being exhibited:

Glandular proliferation in the female breast during puberty and pregnancy.

A

Physiologic hyperplasia

107
Q

Identify what cell adaptation is being exhibited:

Liver transplantation

A

Physiologic hyperplasia

108
Q

Identify what cell adaptation is being exhibited:

Erythropoietin stimulating bone marrow hemopoiesis

A

Physiologic hyperplasia

109
Q

Identify what cell adaptation is being exhibited:

uterine enlargement during pregnancy

A

hypertrophy and hyperplasia

110
Q

Identify what cell adaptation is being exhibited:

Endometrial hyperplasia due to an excess in estrogen

A

Pathologic hyperplasia

111
Q

Identify what cell adaptation is being exhibited:

Prostatic enlargement due to an excess in androgens

A

Pathologic hyperplasia

112
Q

Distinct from cancer but may be fertile soil in which cancerous proliferations may
eventually arise

A

Pathologic hyperplasia

113
Q

Hyperplasia which increases risk for endometrial cancer

A

endometrial hyperplasia

114
Q

causes epithelial hyperplasia which may be a precursor for cancer

A

papillomaviruses

115
Q

neurons that most suscpetible to hypoxic injury than others

A 
Purkinje cells (cerebellum)
neurons of hippocampus
116
Q

ocular disorder of premature infants that leads to blindness which is caused by oxygen toxicity

A

Retrolental fibroplasias (retinopathy of prematurity)

117
Q

syndrome that is caused by alveolar damage due to oxygen toxicity

A

Adult Respiratory Distress Syndrome

118
Q

Classic ultrastructural markers of barbiturate intoxication in hepatocytes which is due to free radical injury caused by drugs and chemicals

A

Proliferation and hypertrophy of the SER

119
Q

Ranges from viruses, bacteria, fungi, and higher forms of parasite that cause cell injury

A

Infectious agents

120
Q

Endogenous self-antigens are responsible for autoimmune diseases causing cell injury

A

immune system

121
Q

Cause of cell injury that can lead to clinical phenotypes ranging from congenital malformations and deficient protein function.

A

genetic abnormalities

122
Q

All stresses and noxious influences exert their effects first at the:

A

molecular and biochemical level

123
Q

Time lag between stress and Histochemical and Ultrastructural changes of cell injury

A

minutes to hours after injury

124
Q

Ischemia of myocardial cell immediate alterations

A

minutes - cell swelling
an hour or two- irreversible
4-12 hours after- unmistakable light microscopic changes

125
Q

5 possible causes of reversible cell injury

A
  1. Decreased ATP generation
  2. Loss of cell membrane integrity
  3. Defects in protein synthesis
  4. Cytoskeletal damage
  5. DNA damage
126
Q

5 ultrastructural alterations of reversible cell injury

A
  1. swelling of cells causing blebbing, blunting and loss of microvilli
  2. ER dilation with detachment of polyribosomes
  3. intracytoplasmic myelin figures
  4. swelling of mitochondria and and appearance of amorphous densitiws
  5. clumping of nuclear chromatin
127
Q

2 light microscopic alterations in morphology of cell injury

A
  1. cellular swelling

2. fatty change

128
Q

3 manifestations of cellular swelling on the whole organ

A

pallor

increased turgor and weight

129
Q

2 manifestations of cellular swelling in light microscopy

A
  1. hydropic change or vacuolar degeneration (small clear vacuoles in the cytoplasm which are opinched off segements of ER
  2. increased eosinophilic staining
130
Q

manifested by appearance of lipid vacuoles in the cytoplasm

A

fatty change

131
Q

Necrosis that occurs as part of granulomatous inflammation and is a manifestation of partial immunity

A

Caseous necrosis

132
Q

The partial immunity in causeous necrosis is caused by the interaction of

A

T Lymphocytes
macrophages
cytokines

133
Q

T lymphocytes involved in causeous necrosis

A

CD4+
CD8+
CD4-CD8-

134
Q

causeous necrosis combines features of

A

coagulative necrosis and liquefactive necrosis

135
Q

Consistency of causeous necrosis

A

cheese-like, friable white appearance

136
Q

appearance of causeous necrosis in histologic examination

A

amorphous eosinophilic appearance

137
Q

Leading cause of causeous necrosis

A

tuberculosis

138
Q

Necrosis that most often affects the lower extremities or bowel and is secondary to vascular occlusion

A

gangrenous necrosis

139
Q

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

A

gangrenous necrosis

140
Q

Gangrenous necrosis that is complicated by infective heterolysis and consequent liquefaction

A

wet gangrene

141
Q

gangrenous necrosis that is primarily characterized by coagulative necrosis without liquefaction

A

dry gangrene

142
Q

Gangrenous necrosis that is caused by Clostridium perfringens which produces gas and a feeling of crepitus

A

gas gangrene

143
Q

Gangrenous necrosis that is caused by Clostridium perfringens which produces gas and a feeling of crepitus (popping)

A

gas gangrene

144
Q

Necrosis that is often associated with immune-mediated vascular damage

A

Fibrinoid necrosis

145
Q

Fibrinoid necrosis occurs when

A

complexes of antigens and antibodies are deposited in the walls of arteries

146
Q

The deposition in the arteril walls are

A

smudgy and acidophilic fibrin-like proteinaceous material

147
Q

Necrosis that occurs in two forms

A

Fat necrosis

148
Q

Two forms of fat necrosis

A

traumatic fat necrosis

enzymatic fat necrosis

149
Q

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

A

Traumatic fat necrosis

150
Q

Fat necrosis which is a complication of acute hemorrhagic pancreatitis (a severe inflammatory disorder of the pancreas)

A

enzymatic fat necrosis

151
Q

pancreatic enzymes that diffuse into inflamed tissue and literally digest the parenchyma

A

proteolytic and lipolytic pancreatic enzymes

152
Q

liberated by the digestion of fat in the pancreas

A

fatty acids

153
Q

process wherein liberated fatty acids form calcium soaps which erode vessels and cause hemorrhage

A

saponification

154
Q

Groas appearance of enzymatic fat necrosis

A

visibly chalky. white areas enable lesion identification

155
Q

histological morphology of enzymatic faat necrosis

A

shadowy outlines of necrotic fat cells
with basophili calcium deposits
surrounded by imflammatroy reaction

Histopathologic and Cytologic Techniques (6 decks)

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