Unit 2 Part 2 Flashcards
(104 cards)
1
Q
Study of disease
A
Pathology
2
Q
infection, genetic etc. and often mutifactoral
A
Etiology of cause
3
Q
Progression of disease
A
Pathogenesis
4
Q
Signs and symptoms
A
Clinical manifestations
5
Q
Pathology 4 studies
A
Etiology
Pathogenesis
Molecular and morphologic changes
Clinical manifestations
6
Q
Structural and functional units of tissues and organs
A
Cells
7
Q
Capable of adjusting their structure and functions in response to physiological and pathological conditions
A
Cell adaptation
8
Q
New steady state
Preserving viability
A
Adaptation
9
Q
Cell poliferation (3 variables)
A
Labile
Stable
Permanent
10
Q
Continously dividing
A
Labile cells
11
Q
Labile cells example
A
Epithelium
Bone marrow
Hematopoietic cells
12
Q
Quiescent
In g0 stage
A
Stable cells
13
Q
Stable cells example
A
Hepatocytes
Smooth muscle
Lmphocytes
14
Q
Nondividing
A
Permanent cells
15
Q
Permanent cells example
A
Neurons
Skeletal and cardiac muscle
16
Q
Types of adaptations are conrolled by
A
Complex molecular mechanisms
17
Q
Types of cellular adaptation
A
Hypertrophy
Hyperplasia
Atrophy
Metaplasia
Dysplasia*
18
Q
normal stressor/stimuli; results in enhanced function
A
Phsyiologic adaptation
19
Q
abnormal stressor/stimuli; results in dysfunction and mortality
A
Pathologic
20
Q
adaptation to positively counteract reduction in function
A
Compensatory adaptation
21
Q
Increase in size; organ enlargement
No new cells
Increase in mrna and proteins
A
Hypertrophy
22
Q
in response to increased demands
seen in cells that cannot divide
changes usually revert to normal if cause is removed
A
Hypertrophy
23
Q
Gym body
A
Physiologic hypertrophy
24
Q
Heart of patient with long standing hypertension
A
Pathologic hypertrophy
25
Increased number of cells
Co-exist with hypertrophy
Takes place IF cell if capable of replication
Hyperplasia
26
Female breast in puberty and pregnancy
Physiologic hyperplasia
27
Excessive hormonal stimulation
Pathologic hyperplasia
28
Hypertrophy and hyperplasia example
Gravid uterus during pregnancy
29
Loss of substance-Shrinkage in the size of cell
Sufficient number of cells is involved
Entire tissue or organ diminishes in size
Not dead
Atrophy
30
Atrophy results from both
Decreased protein synthesis
Increased protein degradation
31
Lysosomes with hydrolytic enzymes
Ubiquitin-proteasome pathway
Increased protein degradation
32
Brain atrophy
Uterus atrophy
Physiologic atrophy
33
Inadequate nutrition (malnutrition)
Diminished blood supply
Pathologic atrophy
34
-Reversible change
-Adult cell type is replaced by another cell type for adverse envi
-occurs in response to stress or chronic irritation
Metaplasia
35
Mechanisms of metaplasia
Re-programming of stem cells
Induced by cytokines, growth factors, envi signals
Retinoic acid may play a role
Unknown exact mechanism
36
Metaplasia SOM
Squamous
Osseous
Myeloid
37
Cigarette smoking
Gastroesophageal reflux disease
Glandural epithelium
Squamous metaplasia
38
TRUE OF FALSE
Atrophy, hypertrophy, hyperplasia, and metaplasia are reversible changes
TRUE
39
TRUE OR FALSE
Hyperplasia and Metaplasia are not premalignant changes
TRUE
40
Fertile fields for dysplasia
Hyperplasia and metaplasia
41
Atypical proliferative changes
due to chronic irritation or inflammation
Cells vary in size and shape
Large nuclei
Increased rate of mitosis
Premalignant change
Dysplasia
42
Cells are undiferrentiated w nuclear and cell structures and mitotic figures
Cancer and tumor is the basis for grading its aggressiveness
Anaplasia
43
New growth
Tumor
Neoplasia
44
Less serious cancer cells
Do not spread and are not life threatening (except in the brain)
Benign
45
Progressive cancer cells
Malignant
46
Failure of cell production
During fetal development, it results to agenesis
Aplasia
47
Absence of an organ due to failure of production
Agenesis
48
Incomplete development of an organ
Decrease in cell production
Hypoplasia
49
Examples of hypoplasia
Hypoplastic left ventricle
Hypoplastic kidney
50
control the composition of their immediate environment and intracellular milieu within a narrow range of physiological parameters
homeostasis
51
denotes pathologic changes that can be reversed when the stimulus is removed, or if the cause of injury is mild
Reversible cell injury
52
denotes pathologic changes that are permanent and cause cell death
Irreversible injury
53
oxygen deprivation
Hypoxic Cell injury
54
loss of blood supply
more rapidly and severely injures
Ischemia
55
cardiorespiratory failure
Inadequate oxygenation
56
anemia, carbon monoxide poisoning
Loss of oxygen carrying capacity of blood
57
Causes of Cellular Injury
Hypoxic Cell injury
a. Ischemia
b. Inadequate oxygenation
c. Loss of oxygen carrying capacity of blood
58
High Susceptibility of Cells to Hypoxic Injury
Neurons (3-4 min)
59
Intermediate Susceptibility of Cells to Hypoxic Injury
Myocardium, hepatocytes, renal epithelium (30 min-2hr)
60
Low susceptibility of cells to hypoxic injury
Fibroblasts, epidermis, skeletal
muscle (many hours)
61
ROS
Hydroxyl, Hydrogen, Superoxide
62
-with a single unpaired electron in an outer orbital
-Chemically unstable=chemical damage
- Initiate autocatalytic reactions
Free Radical Injury
63
If not adequately neutralized, free radicals
can damage cells by
Lipid peroxidation of membranes
DNA fragmentation
Protein cross-linking
64
double bonds in polyunsaturated
membrane lipids are vulnerable
Lipid peroxidation of membranes
65
react with thymine in nuclear and mitochondrial
DNA fragmentation
66
promote sulfhydryl-mediated protein cross
linking
Protein cross-linking
67
Neutralization of Free Radicals
SpoSuGCaEn
1. Spontaneous decay
2. Superoxide dismutase
3. Glutathione (GSH)
4. Catalase
5. Endogenous and exogenous antioxidants
(Vitamins E, A, C and β carotene)
68
cellular injury trauma, heat, cold,
radiation, electric shock
physical agents
69
-Therapeutic drugs - paracetamol
-Nontherapeutic agents – lead, alcohol
-Binding of mercuric chloride to sulfhydryl
groups of proteins
-Generation of toxic metabolites such as
conversion of CCl4 to CCL3* free radicals in
the SER of the liver
Chemical Agents
70
Causes of Cellular Injury
Infectious Agents
ViBaFuRiBaFuPa
a) Viruses
b) Bacteria
c) Fungi
d) Rickettsiae
e) Bacteria
f) Fungi
g) Parasites
71
direct effects of
bacterial toxins; cytopathic effects of
Infectious agents
72
-interfering with DNA,RNA, proteins, cell
membranes or
-inducing apoptosis.
-indirect effects via the host immune reaction.
infectious agents
73
anaphylaxis, loss of
immune tolerance leading to autoimmunity
Immune System -
74
sickle cell
disease, inborn errors of metabolism
Genetic Abnormalities
75
vitamin deficiencies, obesity leading to type II DM, fat leading to atherosclerosis
Nutritional imbalances
76
degeneration as a result of
trauma, intrinsic cellular senesence
Aging
77
causes of cell injury
Hypoxic Cell injury
Free Radical Injury
Physical Agents
Chemical Agents
Infectious Agents
Immune System
Genetic Abnormalities
Nutritional imbalances
Aging
78
2 ways of cell death
necrosis
apoptosis
79
-produced by enzymatic digestion of dead
cellular elements
-irreversible injury
necrosis
80
eliminate unwanted cells--an internally programmed series of events effected
Apoptosis
81
-Morphologic expression of cell death
-disintegration of cell structure
-initiated by overwhelming stress
-elicits an acute inflammatory cell
response
Necrosis
82
types of necrosis
CoLiCaGaFiFa
coagulative
liquefactive
caseous
gangrenous
fibrinoid
fat
83
seen in hypoxic environments
the outline of the dead cells are maintained the tissue is somewhat firm.
◼Example: myocardial infarction
Coagulative necrosis
84
dead cells undergo disintegration and affected tissue is liquified
associated with cellular destruction
and pus formation
ischemia in the brain
Example: cerebral infarction
Liquefactive necrosis
85
ischemia
restriction of blood supply
86
form of coagulation (cheese-like)
caused by mycobacteria
Example: tuberculosis lesions.
Caseous necrosis
87
(secondary to ischemia)
usually with superimposed infection
Example: necrosis of distal limbs, usually foot
and toes in diabetes.
Gangrenous Necrosis
87
(secondary to ischemia)
usually with superimposed infection
Example: necrosis of distal limbs, usually foot
and toes in diabetes.
Gangrenous Necrosis
88
by immune-mediated vascular damage.
by deposition of fibrin-like proteinaceous material in arterial walls
smudgy and eosinophilic
Fibrinoid necrosis
88
by immune-mediated vascular damage.
by deposition of fibrin-like proteinaceous material in arterial walls
smudgy and eosinophilic
Fibrinoid necrosis
89
release of powerful enzymes which damage fat by the production of soaps
chalky white
fat necrosis
89
release of powerful enzymes which damage fat by the production of soaps
chalky white
fat necrosis
90
fat necrosis types
Traumatic fat necrosis
Enzymatic fat necrosis
91
necrosis of fat by pancreatic enzymes.
Enzymatic fat necrosis
92
is restricted to necrosis involving spirochaetal infections (e.g. syphilis).
Gummatous necrosis
93
blockage of the venous drainage (e.g. in
testicular torsion).
Haemorrhagic necrosis
94
-Regulated suicide program
-Controlled by specific genes.
-Fragmentation of nucleus, DNA
-Blebs form and apoptotic bodies are released.
-Apoptotic bodies are phagocytized.
-No neutrophils.
Apoptosis
95
n cells produced =n cells die
Development and morphogenesis
Homeostasis
Deletion of damaged/ dangerous cells
apoptosis
96
During limb formation separate digits evolve
Ablation of cells no longer needed (tadpole)
Apoptosis: Development and morphogenesis
97
Immune system
>95% T and B cells die during maturation
(negative selection)
apoptosis: Homeostasis
98
Examples of Apoptosis
removal of excess cells during embryogenesis
maintain cell population (skin)
eliminate immune cells
remove damaged cells
eliminate cells with DNA damage
Hormone-dependent involution
Cell death in tumours.
99
causes of apoptosis
◼ Physiologic
◼ Pathologic
100
Physiologic Apoptosis
Embryogenesis and fetal development
Hormone dependent involution - mens
Cell loss in proliferating cell populations
Elimination of self-reactive lymphocytes
Death of cells
programmed cell destruction in
embryogenesis
101
Pathologic Apoptosis
DNA damage due to radiation
misfolded proteins
viral infections hiv
Organ atrophy after duct obstruction
