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
2
Q
2 Traditional Divisions of Pathology
A
General Pathology
Systemic Pathology
3
Q
division of pathology concerned with common reactions of cells and tissue to injurious stimuli
not tissue specific
A
General Pathology
4
Q
division of pathology that examines the alterations and underlying mechanisms in organ specific diseases
A
Systemic pathology
5
Q
4 aspects of disease process that form the core of pathology:
A
- etiology
- pathogenesis
- morphologic changes
- clinical manifestations
6
Q
refers to the cause of disease
A
etiology
7
Q
two general kinds of etiology
A
genetic and acquired
8
Q
etiology that includes inherited mutations, and disease associated gene variants, or polymorphisms
A
genetic
9
Q
refers to the sequence of biochemical and molecular events that follow the exposure of cells or tissues to injurious agent
A
pathogenesis
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
11
Q
pathology that traditionally uses morphologic changes to determine the nature of a disease and to follow its progression
A
diagnostic pathology
12
Q
refers to the functional consequences of the disease
A
clinical manifestations
13
Q
clinical manifestation that is objective and can be identified by another person (e.g. 39°C body temperature)
A
sign
14
Q
clinical manifestation that is subjective and cannot be identified by anyone else.
A
symptoms
15
Q
refers to the pathophysiological response to internal and external factors
A
disease
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
17
Q
Refers to a disease or a disorder that has more than one identifying feature or symptom.
A
syndrome
18
Q
refers to the determination of the nature of a disease expressed in a concise manner
A
diagnosis
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
20
Q
disease that has a sudden onset or rapid course (less than a month)
A
acute
21
Q
disease that has a slow onset or a long duration
A
chronic
22
Q
Acute or chronic?
UPPER REPIRATORY TRACT INFECTION
A
acute
23
Q
Acute or chronic?
APPENDICITIS
A
acute
24
Q
Acute or chronic?
ASTHMA
A
Chronic
25
Acute or chronic?
| BRONCHITIS
acute
26
Acute or chronic?
| COPD
chronic
27
a disease with no identifiable cause or have limited literature describing the methodology to define it and has no clear diagnostic criteria.
idiopathic
28
pathology caused by a physician and their treatment (retained forceps after surgery)
iatrogenic
29
infection acquired outside a health care facility.
Community acquired infection
30
refers to hospital acquired infections
nosocomial
31
nosocomial infections should occur within __________ of hospital admission, _________ of discharge or ________ 30 days of operation
48 hours, 3 days, 30 days
32
Diseases that are not transmitted through contact with an infected or afflicted person.
Non communicable diseases (NCD)
33
4 main types of NCDs
1. Cancer
2. Cardiovascular diseases
3. Chronic Respiratory diseases (Asthma and COPD)
4. Diabetes
34
diseases that can be spread from one organism to another, including spread from one person to person or animal to humans
communicable diseases
35
animal to person transmission
zoonotic
36
to affect of contaminated someone with pathogenic microorganisms.
infectious
37
refers to spread of disease through direct bodily contact with an infected person, their discharges or an object or surface they have contaminated.
contagious
38
TRUE OR FALSE?
| All communicable diseases are infectious.
True
39
TRUE OR FALSE?
| All infectious disease are contagious.
FALSE
40
TRUE OR FALSE?
| All contagious diseases are infectious.
TRUE
41
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
cell adaptation
42
4 forms of adaptation in response to environmental stress
1. hypertrophy
2. hyperplasia
3. atrophy
4. metaplasia
43
refers to an increase in the size of the cells resulting into an overall increase of the organ as well
hypertrophy
44
refers to hypertrophy that is due to increase in functional demand or by stimulation by hormones or growth factors
physiologic hypertrophy
45
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.
hyperplasia
46
refers to the decrease in the size of an organ or tissue which results from a decrease in the mass of pre-existing cells.
atrophy
47
5 common causal factors of atrophy
1. disuse
2. nutritional or oxygen deprivation
3. diminshed endocrine stimulation
4. aging
5. denervation
6. pressure
48
intracytoplasmic vacuoles containing debris from degraded organelles which is a characteristic feature of atrophy
autophagic granules
49
refers to the replacement of one differentiated tissue by another
metaplasia
50
metaplasia that replaces columnar epithelium when bronchi, cervix, endometrium, or pancreatic duct are chronically irritated
squamous metaplasia
51
metaplasia which involves formation of new bone at sites of tissue injury
osseous metaplasia
52
metaplasia involving proliferation of hematopoietic tissue at sites other than the bone marrow, such as the liver and spleen
myeloid metaplasia
53
occurs when the limits of adaptive responses are exceeded and cells are exposed to injurious agents or stress, deprived of essential nutrients.
cell injury
54
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.
reversible, irreversible
55
Determine the cellular response given the injurious stimulus:
increased demand or increased stimulation (growth factors & hormones)
hyperplasia, hypertrophy
56
Determine the cellular response given the injurious stimulus:
decreased nutrients or decreased stimulation
atrophy
57
Determine the cellular response given the injurious stimulus:
chronic chemical or physical irritation
metaplasia
58
Determine the cellular response given the injurious stimulus:
acute or transient cell injury
reversible injury
59
Determine the cellular response given the injurious stimulus:
progressive and severe cell injury including DNA damage
irreversible injury + cell death
60
6 causes of cell injury
1. hypoxic cell injury
2. free radical injury
3. chemical cell injury
4. infectious agents
5. immune sytem
6. genetic abnormalities
61
Oxygen deprivation or hypoxia causes cell injury by reducing ________
aerobic oxidative respiration
62
3 causes of hypoxia include:
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)
63
the first cell organelle affected by hypoxic cell injury
mitochondria
64
during a hyposic cell injury, mitochondria undergoes decreased ________ and _________
oxidative phosphorylation and ATP synthesis
65
4 events of early stage hypoxic cell ijury
1. mitochondria affected
2. intracellular swelling (due to decreased ATP causing failure of pump)
3. ribosome disaggregation
4. acidification and clumping nuclear chromatin
66
2 morphologic signs of reversible hypoxic injury
1. formation of myelin figures (whorl like structures from damaged membrane)
2. cell blebs (surface deformity due to cytoskeleton disfunction)
67
3 morphologic signs of irreversible hypoxic cell injury
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
hypoxic injury becomes irreversible in neurons after ___________
3-5 minutes
69
hypoxic cell injury becomes irreversible to myocardial cells and hepatocytes after ___________
1-2 hours
70
hypoxic cell injury becomes irreversible to skeleltal muscle cells after ___________
many hours
71
injury caused by molecules that have a single unpaired electron in the outer orbital
free radical injury
72
examples of free radicals
1. superoxide
| 2. hydroxyl radicals
73
three mechanisms that degrade free radicals
1. intracellular enzymes
2. exogenous and endogenous antioxidants
3. spontaneous decay
74
two contrasting morphologic patterns of cell death
1. necrosis
| 2. apoptosis
75
it is the sum of the degradative and inflammatory reactions occurring after tissue death caused by injury
necrosis
76
The causes of necrotic morphology are:
1. denaturation of intracellular proteins
| 2. enzymatic digestion of lethally injured cells
77
2 enzymatic processes that digest the necrotic cell
1. autolysis
| 2. heterolysis
78
refers to degradative reactions in cells caused by intracellular enzymes from lysozomes indigenous to the cell
autolysis
79
occurs after the death of the organism and is not considered necrosis
postmortem autolysis
80
It refers to cellular degradation by enzymes derived from sources extrinsic to the cell like leucocytes or macrophages
heterolysis
81
necrosis, due to leaking content from inability to maintain membrane integrity, causes ________
inflammation
82
The earliest histologic evidence of myocardial necrosis does not become apparent until
4-12 hours
83
When large numbers of cells die the tissue or organ is said to be
necrotic
84
Necrosis that results most often from a sudden cutoff of blood supply to an organ (ischemia), particularly the heart and kidney (solid organs).
coagulative necrosis
85
The eosinophilic anucleate appearance of the cell due to intense intracellular acidosis denaturing structural proteins and releasing proteolytic enzymes from the lysosome
“
Tombstone appearanceof the cells.
86
3 nuclear changes which are the morphologic of irreversible cell injury and necrosis
1. Pyknosis
2. Karyorrhesis
3. Karyolysis
87
Nuclear change where chromatin clumps and shrinks with increased basophilia
pyknosis
88
Nuclear change involving fragmentation of chromatin
karyorrhexis
89
Nuclear change involving fading of chromatin material and disappearance of stainable nuclei
karyolysis
90
Necrotic cells in coagulative necrosis are removed by
heterolysis of leukocytes
91
A localized area of coagulative necrosis is called
infarct
92
Necrosis that results to characteristic digestion, softening, and liquefaction of tissue.
Liquefactive necrosis
93
Liquefaction is caused by
autolysis
94
examples of liquefactive necrosis
1. ischemic injury to CNS
2. focal bacteria
3. fungal infections
95
creamy yellow necrotic material made of liquefied tissue debris and neutrophils
pus
96
mechanisms that generate free radicals
a. Normal metabolism
b. Oxygen toxicity
c. Ionizing radiation
d. Ultraviolet light
e. Drugs and chemicals
f. Reperfusion after ischemic injury
97
mechanisms that generate free radicals
a. Normal metabolism
b. Oxygen toxicity
c. Ionizing radiation
d. Ultraviolet light
e. Drugs and chemicals
f. Reperfusion after ischemic injur
98
What happens to normal cells when put under stress?
adaptation
99
If the cell was unable to adapt in response to stress or injurious stimulus, what happens?
cell injury
100
Refers to cell injury that is mild or transient
reversible injury
101
Refers to cell injury that is mild or transient
reversible injury
102
Refers to cell injury that is severe or progressive
irreversible cell injury
103
Identify what cell adaptation is being exhibited:
| Increase workload among body builders
physiologic hypertrophy
104
Identify what cell adaptation is being exhibited:
| estrogenic hormone induced increase in the uterine size during pregnancy
Physiologic hypertrophy
105
Identify what cell adaptation is being exhibited:
| Hemodynamic overload due to hypertension of faulty valves
Pathologic hypertrophy
106
Identify what cell adaptation is being exhibited:
| Glandular proliferation in the female breast during puberty and pregnancy.
Physiologic hyperplasia
107
Identify what cell adaptation is being exhibited:
| Liver transplantation
Physiologic hyperplasia
108
Identify what cell adaptation is being exhibited:
| Erythropoietin stimulating bone marrow hemopoiesis
Physiologic hyperplasia
109
Identify what cell adaptation is being exhibited:
| uterine enlargement during pregnancy
hypertrophy and hyperplasia
110
Identify what cell adaptation is being exhibited:
| Endometrial hyperplasia due to an excess in estrogen
Pathologic hyperplasia
111
Identify what cell adaptation is being exhibited:
| Prostatic enlargement due to an excess in androgens
Pathologic hyperplasia
112
Distinct from cancer but may be fertile soil in which cancerous proliferations may
eventually arise
Pathologic hyperplasia
113
Hyperplasia which increases risk for endometrial cancer
endometrial hyperplasia
114
causes epithelial hyperplasia which may be a precursor for cancer
papillomaviruses
115
neurons that most suscpetible to hypoxic injury than others
```
Purkinje cells (cerebellum)
neurons of hippocampus
```
116
ocular disorder of premature infants that leads to blindness which is caused by oxygen toxicity
Retrolental fibroplasias (retinopathy of prematurity)
117
syndrome that is caused by alveolar damage due to oxygen toxicity
Adult Respiratory Distress Syndrome
118
Classic ultrastructural markers of barbiturate intoxication in hepatocytes which is due to free radical injury caused by drugs and chemicals
Proliferation and hypertrophy of the SER
119
Ranges from viruses, bacteria, fungi, and higher forms of parasite that cause cell injury
Infectious agents
120
Endogenous self-antigens are responsible for autoimmune diseases causing cell injury
immune system
121
Cause of cell injury that can lead to clinical phenotypes ranging from congenital malformations and deficient protein function.
genetic abnormalities
122
All stresses and noxious influences exert their effects first at the:
molecular and biochemical level
123
Time lag between stress and Histochemical and Ultrastructural changes of cell injury
minutes to hours after injury
124
Ischemia of myocardial cell immediate alterations
minutes - cell swelling
an hour or two- irreversible
4-12 hours after- unmistakable light microscopic changes
125
5 possible causes of reversible cell injury
1. Decreased ATP generation
2. Loss of cell membrane integrity
3. Defects in protein synthesis
4. Cytoskeletal damage
5. DNA damage
126
5 ultrastructural alterations of reversible cell injury
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
2 light microscopic alterations in morphology of cell injury
1. cellular swelling
| 2. fatty change
128
3 manifestations of cellular swelling on the whole organ
pallor
| increased turgor and weight
129
2 manifestations of cellular swelling in light microscopy
1. hydropic change or vacuolar degeneration (small clear vacuoles in the cytoplasm which are opinched off segements of ER
2. increased eosinophilic staining
130
manifested by appearance of lipid vacuoles in the cytoplasm
fatty change
131
Necrosis that occurs as part of granulomatous inflammation and is a manifestation of partial immunity
Caseous necrosis
132
The partial immunity in causeous necrosis is caused by the interaction of
T Lymphocytes
macrophages
cytokines
133
T lymphocytes involved in causeous necrosis
CD4+
CD8+
CD4-CD8-
134
causeous necrosis combines features of
coagulative necrosis and liquefactive necrosis
135
Consistency of causeous necrosis
cheese-like, friable white appearance
136
appearance of causeous necrosis in histologic examination
amorphous eosinophilic appearance
137
Leading cause of causeous necrosis
tuberculosis
138
Necrosis that most often affects the lower extremities or bowel and is secondary to vascular occlusion
gangrenous necrosis
139
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
gangrenous necrosis
140
Gangrenous necrosis that is complicated by infective heterolysis and consequent liquefaction
wet gangrene
141
gangrenous necrosis that is primarily characterized by coagulative necrosis without liquefaction
dry gangrene
142
Gangrenous necrosis that is caused by Clostridium perfringens which produces gas and a feeling of crepitus
gas gangrene
143
Gangrenous necrosis that is caused by Clostridium perfringens which produces gas and a feeling of crepitus (popping)
gas gangrene
144
Necrosis that is often associated with immune-mediated vascular damage
Fibrinoid necrosis
145
Fibrinoid necrosis occurs when
complexes of antigens and antibodies are deposited in the walls of arteries
146
The deposition in the arteril walls are
smudgy and acidophilic fibrin-like proteinaceous material
147
Necrosis that occurs in two forms
Fat necrosis
148
Two forms of fat necrosis
traumatic fat necrosis
| enzymatic fat necrosis
149
Fat necrosis that occurs after a severe injury to tissue with high fat content, such as the breast.
Traumatic fat necrosis
150
Fat necrosis which is a complication of acute hemorrhagic pancreatitis (a severe inflammatory disorder of the pancreas)
enzymatic fat necrosis
151
pancreatic enzymes that diffuse into inflamed tissue and literally digest the parenchyma
proteolytic and lipolytic pancreatic enzymes
152
liberated by the digestion of fat in the pancreas
fatty acids
153
process wherein liberated fatty acids form calcium soaps which erode vessels and cause hemorrhage
saponification
154
Groas appearance of enzymatic fat necrosis
visibly chalky. white areas enable lesion identification
155
histological morphology of enzymatic faat necrosis
shadowy outlines of necrotic fat cells
with basophili calcium deposits
surrounded by imflammatroy reaction
