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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
Q

Metaplasia examples

A

-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

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26
Q

barret’s esophagus

A

?

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27
Q

Dysplasia

A

-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.

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28
Q

Dysplasia causes

A

-chronic inflammation and irritation

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29
Q

Dysplasia location

A

-metaplastic squamous epithelium in respiratory tract and uterine cervix

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30
Q

PAP smear

A

-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

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31
Q

8 Causes of cell injury

A
  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
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32
Q

Causes of oxygen deprivation

A

-hypoxia
-ischemia

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33
Q

hypoxia

A

-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
Q

ischemia

A

-loss of oxygenated blood supply to tissues

35
Q

nutritional imbalances

A

-typically indirect causes of injury
-nutritional deficiencies (caloric or vitamin)
-excess nutrition
-diabetes
-artheroclerosis

36
Q

Diabetes

A

-can be caused by obesity
-excess blood sugar levels can damage cells

37
Q

Artherosclerosis

A

-can be caused by diet rich in fats
-can result in blockage of coronary arteries

38
Q

Aging

A

-accumulation of damage by ROS
-loss of telomerase function

39
Q

Uterus enlargement during pregnancy is mainly caused by:

A

-hormone-induced hypertrophy of uterus smooth muscle cells

40
Q

Which of the following may develop into cancer?

-hyperplasia
-hypertrophy
-metaplasia

A

-hyperplasia and metaplasia

41
Q

Hyperplasia is likely caused by:

A

-Increased workload
-Increased growth factors or hormones
-Chronic irritation
-Increased protein synthesis

42
Q

The liver has a very high capacity to regenerate after surgical
resection. This is caused by:

A

an increased proliferation of the remaining hepatocytes

43
Q

Reversible cell injury

A

-decrease in cell function

44
Q

irreversible cell injury

A

-cell death
-structural changes
-microscopic changes
-gross morphologic changes

45
Q

Metaplasia is a precursor to

A

-malignancy
-May be caused by reprogramming of stem cells rather than by
transdifferentiation of mature cells

46
Q

What kind of
metaplasia in
stomach may occur
if pyloric sphincter is weak?

A

-intestinal metaplasia

47
Q

Pathologic hyperplasia

A

– typically the result of excessive hormonal or growth factor
stimulation
– hyperplastic tissue may eventually become malignant

48
Q

Ischemia in myocardial cells

A

-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
Q

characteristics of REVERSIBLE injury

A

-cellular swelling
-fatty change

50
Q

cellular swelling

A

-result of failure of energy-dependent ion pumps in the plasma membrane
=inability to maintain ionic and fluid homeostasis

51
Q

fatty change

A

-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
Q

Characteristics of Irreversible injury

A

-Inability to reverse mitochondrial dysfunction (lack of oxidative
phosphorylation and ATP generation)
-Profound disturbances in membrane function (membrane
dysfunction)

53
Q

Reversible cell injury mech

A

-cell is injured
-swelling of ER and mitochondria
-memnrane blebs
-clumping of chromatin
-recovery = normal cell

PIC

54
Q

Mechanisms of Cell Injury

A

-ATP depletion
-damage to mitochondria
-influx of calcium
-increased oxidative stress

55
Q

ATP depletion

A

-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
Q

Damage to mitochondria by

A

-increased Ca2+
-ROS
-lipid peroxidation

57
Q

Damage to mitochondria results in

A

-necrosis due to inability to generate ATP (loss of membrane potential)
-apoptosis by cytochrome c

58
Q

2 ways to increase cytosolic calcium concentration

A

-release from intracellular calcium stores
-influx across plasma membrane

59
Q

Influx of calcium mech of damage

A

-activate various enzymes
=decreased ATP, membrane damage, chromatin damage

60
Q

Increased oxidative stress

A

-generation of ROS by:
-inflammation
-radiation
-chemicals
-reperfusion injury

PIC

61
Q

Mechs of OFR and ROS damage

A

-lipid peroxidation
-DNA fragmentation
-protein oxidation and cross-linking

62
Q

lipid peroxidation of membranes

A

-C=C bonds attacked
-peroxidated membrane lipids are less hydrophobic
=converts lipids to detergents
=membrane integrity reduced

63
Q

DNA fragmentation

A

-Thymine (per)oxidation: base pairing between T and A altered = mutation from repair
-ssDNA breaks: breakage of phosphodiester backbone = reduced replication and transcription

64
Q

Protein oxidation and cross-linking (C&M residues)

A

-altered protein structure
-increased protein degradation
-loss of enzymatic activity

65
Q

Cellular mechanisms to deal with OFRs and ROS

A

-superoxide dismutase
-glutathione peroxidase
-catalase
-antioxidants
-sequestration of free ionized iron and copper

66
Q

superoxide dismutase

A

radical to peroxide

67
Q

glutathione peroxidase

A
68
Q

catalase

A
69
Q

antioxidants

A

-scavenge (react with) free radicals
-many sold as dietary supplements
-vitamin C and E, B-carotene

70
Q

sequestration of free ionized iron and copper

A

-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
Q

Defects in membrane permeability

A

-mitochondrial, plasma, lysosomal membrane damage

72
Q

mitochondrial membrane damage

A

-decreased ATP production
-necrosis and apoptosis

73
Q

plasma membrane damage

A

-loss of osmotic balance
-influx of fluids and ions
-loss of cellular contents

74
Q

lysosomal membrane damage

A

-leakage of enzymes into cytoplasm
-activation of acid hydrolases in acid pH of injured cells

75
Q

Apoptosis

A

-pathway of cell death
-cells destined to die activate enzymes capable of degrading cells DNA and proteins

76
Q

Physiological causes of apoptosis

A

-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
Q

Pathological causes of apoptosis

A

-DNA damage
-accumulation of misfolded proteins
-cell injury in infection
-pathological atrophy in parenchymal organs after duct obstruction

78
Q

Mechanisms of Apoptosis

A

-intrinsic (mitochondrial)
-extrinsic (death receptor)

79
Q

Mitochondrial (intrinsic) pathway of apoptosis

A

-cell injury
-Bcl-2 effectors interact with mitochondria = dysfunction
-release cytochrome c and pro-apoptotic proteins

80
Q

Death receptor (extrinsic pathway of apoptosis

A
81
Q

Dimerization and oligomerization of Bax or Bak

A

-increases mitochondrial membrane permeability and cytochrome c release

82
Q

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