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PATHO > Lecture 1+2: Cell Injury > Flashcards

Lecture 1+2: Cell Injury Flashcards

1
Q

Cellular responses to stress and injurious stimuli

A

-homeostasis
-adaptation
-cell injury
-cell death

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2
Q

homeostasis

A

-cells maintain intracellular environment within range of physiological parameters

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3
Q

adaptation

A

-cells achieving a new steady state and preserving viability by changing size, number, and form

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4
Q

Adaptation responses

A

-hypertrophy (size)
-hyperplasia (number)
-atrophy (size)
-metaplasia (form)
-dysplasia (organization)

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5
Q

cell injury

A

-when cells are stressed to the point where they can NOT adapt
-reversible or subcellular alterations

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6
Q

cell death

A

-most crucial event in evolution of disease in a tissue or organ

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7
Q

Response of myocardial cells to overload and ischemia

A

-adaptation: leads to hypertrophy
-cell injury: leads to ischemia, reversible injured monocyte and cell death

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8
Q

Hypertrophy

A

-increase in the size of cells
=increase in size of organ

*only increase cell size NOT cell number

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9
Q

Hypertrophy affects

A

-only cells INcapable of dividing
-striated muscle cells in skeletal and cardiac muscle

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10
Q

Hypertrophy causes

A

-increased workload
-physiological stimuli (estrogen enlarging uterus during pregnancy)
-pathological (hypertension)

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11
Q

Hypertrophy is characterized by

A

-increase protein synthesis
-mechanical triggers (stretching)
-hormonal triggers

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12
Q

Physiological hypertrophy

A

-caused by growth signal
-adaptive

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13
Q

pathological hypertrophy

A

-stress signal (hypertension, MI)
-sarcomere mutation
-decompensation
-maladaptive

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14
Q

Hyperplasia

A

-increase in NUMBER of cells
-physiologic or pathologic

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15
Q

Hyperplasia examples

A

-physiologic hormonal
-proliferation of connective tissue during wound healing
-physiologic compensatory

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16
Q

physiologic hormonal hyperplasia

A

-proliferation of female mammary epithelium during puberty

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17
Q

physiologic compensatory hyperplasia

A

-regeneration of partially resected liver by remaining haptocytes

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18
Q

Impact of female hormones on mammary gland (PHYSIOlogical)

A

-estrogen: form TEBs and ductal elongation (puberty)
-progesterone: side branching (adult) and alveologenesis and lactogenic differentiation
-prolactin: alveologenesis and lactogenic differentiation (pregnancy)

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19
Q

Role of hormones in breast cancer (PATHOlogical)

A

-hormone imbalance?

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20
Q

Atrophy

A

-shrinkage in cell size due to loss of substance
=smaller organ

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21
Q

Atrophy causes

A

-decreased workload
-loss of innervation
-reduced blood supply
-inadequate nutrition
-aging (senile atrophy)

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22
Q

Decreased cell size in atrophy is caused by

A

-increased protein degradation
-reduced protein synthesis

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23
Q

Metaplasia

A

-reversible
-one adult cell type is replace by another adult cell type

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24
Q

Metaplasia cause

A

-often response to chronic irritation and inflammation that make cells better able to withstand stress

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25
Metaplasia examples
-Cilliated columnar epithelial cells of trachea and bronchi clear foreign materials and mucous -REPLACED by squamous epithelial cells in smokers (vit A deficiency) =coughing and infections -also barret's esophagus
26
barret's esophagus
?
27
Dysplasia
-deranged cell growth of specific tissue that results in cells that VARY in SIZE, NUMBER, SHAPE, and ORGANIZATION -adaptive in that it is potentially reversible after irritating cause has been removed -strongly implicated as a precursor (precancerous lesion) of cancer.
28
Dysplasia causes
-chronic inflammation and irritation
29
Dysplasia location
-metaplastic squamous epithelium in respiratory tract and uterine cervix
30
PAP smear
-early detection of cervical cancer -look at cervical cells under microscope -every 3 years starting at age 21 -30-65: every 3-5 years with HPV test
31
8 Causes of cell injury
1. Oxygen deprivation 2. Chemical agents – poisons, air pollutants, CO, asbestos 3. Infectious agents – viruses, bacteria, fungi, parasites 4. Immunological reactions – autoimmune diseases 5. Genetic defects – sickle cell anemia, familial hypercholesterolemia 6. Physical agents – trauma, heat, cold, electric shock 7. Nutritional imbalances 8. Aging
32
Causes of oxygen deprivation
-hypoxia -ischemia
33
hypoxia
-oxygen deficiency -inadequate oxygenation of blood = pneumonia -reduction in oxygen-carrying capacity of the blood (blood loss anemia or carbon monoxide poisoning in which CO forms stable complex with hemoglobin that prevents oxygen binding
34
ischemia
-loss of oxygenated blood supply to tissues
35
nutritional imbalances
-typically indirect causes of injury -nutritional deficiencies (caloric or vitamin) -excess nutrition -diabetes -artheroclerosis
36
Diabetes
-can be caused by obesity -excess blood sugar levels can damage cells
37
Artherosclerosis
-can be caused by diet rich in fats -can result in blockage of coronary arteries
38
Aging
-accumulation of damage by ROS -loss of telomerase function
39
Uterus enlargement during pregnancy is mainly caused by:
-hormone-induced hypertrophy of uterus smooth muscle cells
40
Which of the following may develop into cancer? -hyperplasia -hypertrophy -metaplasia
-hyperplasia and metaplasia
41
Hyperplasia is likely caused by:
-Increased workload -Increased growth factors or hormones -Chronic irritation -Increased protein synthesis
42
The liver has a very high capacity to regenerate after surgical resection. This is caused by:
an increased proliferation of the remaining hepatocytes
43
Reversible cell injury
-decrease in cell function
44
irreversible cell injury
-cell death -structural changes -microscopic changes -gross morphologic changes
45
Metaplasia is a precursor to
-malignancy -May be caused by reprogramming of stem cells rather than by transdifferentiation of mature cells
46
What kind of metaplasia in stomach may occur if pyloric sphincter is weak?
-intestinal metaplasia
47
Pathologic hyperplasia
– typically the result of excessive hormonal or growth factor stimulation – hyperplastic tissue may eventually become malignant
48
Ischemia in myocardial cells
-noncontractile after 1-2 min -cell death after 20-30 min -appear dead by electron microscope at 2-3 hours -appear dead by light microscope at 6-12 hours
49
characteristics of REVERSIBLE injury
-cellular swelling -fatty change
50
cellular swelling
-result of failure of energy-dependent ion pumps in the plasma membrane =inability to maintain ionic and fluid homeostasis
51
fatty change
-occurs in hypoxic injury and various forms of toxic or metabolic injury -manifested by appearance of small or large lipid vacuoles in cytoplasm -mainly occurs in cells involved in metabolism such as hepatocytes and myocardial cells
52
Characteristics of Irreversible injury
-Inability to reverse mitochondrial dysfunction (lack of oxidative phosphorylation and ATP generation) -Profound disturbances in membrane function (membrane dysfunction)
53
Reversible cell injury mech
-cell is injured -swelling of ER and mitochondria -memnrane blebs -clumping of chromatin -recovery = normal cell PIC
54
Mechanisms of Cell Injury
-ATP depletion -damage to mitochondria -influx of calcium -increased oxidative stress
55
ATP depletion
-ischemia decreases oxidative phosphorylation in mitochondria =decrease ATP =ER swelling, loss of microvilli, blebs (calcium) =clumping of chromatiin (anaerobic glycolysis decreases pH) =decrease protein synthesis
56
Damage to mitochondria by
-increased Ca2+ -ROS -lipid peroxidation
57
Damage to mitochondria results in
-necrosis due to inability to generate ATP (loss of membrane potential) -apoptosis by cytochrome c
58
2 ways to increase cytosolic calcium concentration
-release from intracellular calcium stores -influx across plasma membrane
59
Influx of calcium mech of damage
-activate various enzymes =decreased ATP, membrane damage, chromatin damage
60
Increased oxidative stress
-generation of ROS by: -inflammation -radiation -chemicals -reperfusion injury PIC
61
Mechs of OFR and ROS damage
-lipid peroxidation -DNA fragmentation -protein oxidation and cross-linking
62
lipid peroxidation of membranes
-C=C bonds attacked -peroxidated membrane lipids are less hydrophobic =converts lipids to detergents =membrane integrity reduced
63
DNA fragmentation
-Thymine (per)oxidation: base pairing between T and A altered = mutation from repair -ssDNA breaks: breakage of phosphodiester backbone = reduced replication and transcription
64
Protein oxidation and cross-linking (C&M residues)
-altered protein structure -increased protein degradation -loss of enzymatic activity
65
Cellular mechanisms to deal with OFRs and ROS
-superoxide dismutase -glutathione peroxidase -catalase -antioxidants -sequestration of free ionized iron and copper
66
superoxide dismutase
radical to peroxide
67
glutathione peroxidase
68
catalase
69
antioxidants
-scavenge (react with) free radicals -many sold as dietary supplements -vitamin C and E, B-carotene
70
sequestration of free ionized iron and copper
-free ionized iron and copper can cause ROS and oxygen free radical production via fenton reaction -transferrin, ferritin, and ceruloplasmin sequester these metal ions and prevent them from causing ROS and OFR production
71
Defects in membrane permeability
-mitochondrial, plasma, lysosomal membrane damage
72
mitochondrial membrane damage
-decreased ATP production -necrosis and apoptosis
73
plasma membrane damage
-loss of osmotic balance -influx of fluids and ions -loss of cellular contents
74
lysosomal membrane damage
-leakage of enzymes into cytoplasm -activation of acid hydrolases in acid pH of injured cells
75
Apoptosis
-pathway of cell death -cells destined to die activate enzymes capable of degrading cells DNA and proteins
76
Physiological causes of apoptosis
-programmed destruction of cells during embryogenesis -involution of hormone-dependent tissue upon hormone deprivation: endometrial cell breakdown during menstrual cycle -cell loss in proliferating cell populations: intestinal crypt epithelia -elimination of potentially harmful self-reactive lymphocytes: before or after their maturation -cell death induced by cytotoxic T lymphocytes
77
Pathological causes of apoptosis
-DNA damage -accumulation of misfolded proteins -cell injury in infection -pathological atrophy in parenchymal organs after duct obstruction
78
Mechanisms of Apoptosis
-intrinsic (mitochondrial) -extrinsic (death receptor)
79
Mitochondrial (intrinsic) pathway of apoptosis
-cell injury -Bcl-2 effectors interact with mitochondria = dysfunction -release cytochrome c and pro-apoptotic proteins
80
Death receptor (extrinsic pathway of apoptosis
81
Dimerization and oligomerization of Bax or Bak
-increases mitochondrial membrane permeability and cytochrome c release
82
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