Flashcards in 54-Breakdown of Homeostasis Deck (66)
1
What is homeostasis
normal steady state
2
What happens when cells encounter physiologic stress
They must adapt, get injured, or die
3
What is the most crucial event in evolution of disease
Cell death
4
What happens after prolonged or severe injury
Cell death-necrosis or apoptosis
5
What are the cellular adaptations to stress
Atrophy
Hypertrophy-physiologic or pathologic
Hyperplasia-physiologic or pathologic
metaplasia
6
What is atrophy
Shrinking of cell to preserve function and survive
7
What is hypertrophy
Cell enlarges, limited capacity to divide
8
What is hyperplasia
More cells are produced if they are capable of replication
9
What is metaplasia
Differentiation from one adult cell type to another
10
What happens to skeletal muscle when it loses its innervation
denervation-atrophy, become small and angular
11
What causes atrophy
Decreased workload
loss of innervation
Diminished blood supply
Inadequate nutrition
Loss of endocrine
aging
12
what is an example of pathologic hypertrophy
Hypertension and enlargement of heart
Muscular Dystrophy
13
What is an example of physiologic hypertrophy
Pregnancy from estrogen
14
What is an example of physiologic hyperplasia
Pregnancy and proliferation of breast tissue
15
What is the difference between hyperplasia and cancer
Hyperplasia is tightly controlled
Cancer has uncontrolled growth
16
What is an example of metaplasia
Chronic smokers
Change of epithelium in branches from columnar to squamous
Gain survival, but loss of protection like mucous secretion and cilia
17
Why does metaplasia occur
One cell type is sensitive to stress and is replaced by a type that can withstand the stress to try to survive
18
What causes cell injury
EVERYTHING
Intrinsic-genetic
Acquired-everything else
19
What does cell response to injurious stimuli depend on
Type, duration, severity
20
What are the consequences of injurious stimulus
Cell type, status, adaptability, genetic make up
21
Where are the sites of vulnerability for cell injury
Mitochondria, calcium, membrane, protein and DNA integrity
22
What are the morphologic changes from injury
Biochemical changes
They are time dependent
23
What does mitochondrial damage lead to
ATP depletion and increase ROS, necrosis and apoptosis
24
ATP depletion is due to what
Decreased oxygen, reduced nutrients, mitochondrial damage, toxins
25
If you have ATP depletion what can you test for
Lactic acidosis in serum blood test
26
Increase ROS leads to what
Damaged lipids, proteins, DNA
27
How does reduced ATP affect cells
Reduced ATP dependent sodium and calcium pumps, anaerobic glycolysis (lactic acid production and decreased pH), disruption of protein synthesis
28
How are ROS formed
Produced normally during redox reactions
Produced by phagocytic leukocytes (neutrophils and Macs) for destroying microbes
29
How does ROS contribute to disease
Cancer-mutation from free radicals
atherosclerosis-plaque formation
Aging-accumulative damage
Toxicology-acetaminophen toxicology
hypoxia
30
What are the sources of calcium
mitochondria, ER, extracellular space
31
What does increased calcium do
activate enzymes which leads to:
Membrane damage
Nuclear damage
Decreased ATP
trigger apoptosis
32
Most important sites of membrane damage are
Mitochondrial, lysosomal, plasma
33
What does damage to lysosomal membranes do
leak enzymes and digest cell components
34
What does damage to DNA and proteins lead to
Accumulation of damaged DNA, misfolded proteins.
35
What happens when damage exceeds repair mechanisms
apoptosis
36
What is ischemia
Decreased blood flow leading to loss of oxygen and nutrients
37
Does ischemic or hypoxic lead to faster injuries
ischemia
38
What is hypoxia
Decreased oxygen delivery, use anaerobic glycolysis as result
39
What happens to oxygen deprived cells
Decreased ATP, mitochondrial damage, accumulation of ROS, Ca influx
40
What happens during the sequence of changes in cell injury
Quickly lose cell function, but still reversible injury
Death and irreversible, biochemical alterations
ultrastructural changes (EM)
Light microscope changes (AP)
Gross morphological changes
41
How can you reverse cell injury
During early stages if damaging stimulus is removed
42
What are the 2 morphological correlates in reversible injury
Cell swelling
Fatty change
43
What causes cell swelling in reversible injuries
Failure of energy ion pumps, inability to maintain ionic and fluid homeostasis
44
What happens in reversible cell swelling
Loss of microvilli, swollen mitochondria, membrane blebbing
45
What happens in fatty change
Clear lipid vacuoles in cells participating in fat metabolism, caused from chronic alcohol use
46
What 2 characteristics cause irreversibility
Cannot correct mitochondria dysfunction
Profound disruption of membranes
47
What are the common early changes in necrosis
hypereosinophilia-really pink
vacuolization
Nuclear changes (pkynosis, karyorrhexis, karyolysis, disappearance)
48
What are the later changes in necrosis
Coagulation and liquefaction
49
What is coagulative necrosis
autolysis-intrinsic source
Preservation of cell outlines
50
What is a type of coagulative necrosis
Myocardial infarction, ischemic injury
51
What is liquefactive neccrosis
heterolysis-extrinsic source
Loss of cell outline
52
What is a type of liquefactive necrosis
Bacterial abscess
53
What is caseous necrosis
TB infection!!
Cheese like appearance
Aggregate of granular pink material
tissue architecture obliterated
54
What is fat necrosis
Fat destruction from release of pancreatic lipases, liquefy membranes of fat cells
Microscopically-shadowy outline with basophilic calcium deposits
55
What is fibrinoid necrosis
Immune reaction with antigens and antibodies in walls of arteries
Bright pink appearance
56
What is dystrophic calcification
Calcification in dead or dying tissues, seen in plaques
57
What causes intracellular accumulation
Abnormal metabolism
Abnormal protein folding and transport
enzyme defect
Incomplete lysosomal degradation
58
What are some intracellular accumulations
Lipids, proteins, glycogen, pigments
59
What accumulates in Alzheimer's
tau proteins
60
Is necrosis physiologic or non physiologic
ALWAYS PATHOLOGIC
61
What are the 2 ways to initiate apoptosis
Mitochondrial/intrinsic
Death receptor/extrinsic
62
nonmorphologic characteristics of necrosis
Pathologic, no gene transcription, unregulated, no energy, lysosome disruption, cell membrane leakage
63
Non morphologic characteristics of apoptosis
Physiologic and non physiologic
Gene transcription
Highly regulated
Needs energy
Cleave chromatic
Lysosome intact
cell membrane intact
64
Morphologic characteristics of necrosis
Death of groups
karyolysis and karyorrhexis
organelles destroyed
Swelling
Inflammatory response
65
Morphologic characteristics of apoptosis
Death in individual cells
Chromatic clumping
Organelles preserved
Cell shrinkage
No inflammation
66