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Patho Exam 4 > Hudmon > Flashcards

Hudmon Flashcards

1
Q

What are cellular responses to stress and injurious stimuli?

A

-homeostasis
-adaptation
-cell injury
-cell death

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2
Q

Homeostasis

A

cells maintain their intracellular environment within a narrow range of physiological parameters

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3
Q

Adaptation

A

a cells encounter physiological stress or pathological stimuli, they can undergo adaptation, achieving a new steady state and preserving viability and function by changing their size, number, and form

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4
Q

Cell injury

A

occurs when cells are stressed to the point that they are unable to adapt

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5
Q

cell death

A

one of the most crucial events in the evolution of disease in any tissue or organ (e.g. ischemia, infections, toxin, and immune responses)

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6
Q

Hypertrophy

A

an increase in the size of the cells resulting in increase in the size of the organ, there is no increase in cell number

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7
Q

When does hypertrophy occur?

A

It only occurs in cells that are incapable of dividing: striated muscles cells in both the skeletal muscle and the heart

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8
Q

What is the common cause of hypertrophy?

A

Commonly caused by increased workload

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9
Q

What are examples of increased workload in hypertrophy?

A

physiological stimuli (estrogen-induced uterus enlargement during pregnancy)
[and]
pathological conditions (hypertension, aortic valve)

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10
Q

how is hypertrophy charachterized?

A

by an increase in protein synthesis, this may be mechanical triggers (stretching) or hormonal triggers (adrenergic hormones)

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11
Q

Hyperplasia

A

increase in the number of cells (not cell size)

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12
Q

What are examples of physiological hormonal hyperplasia

A

-proliferation of the female mammary epithelium during puberty…hormones (estrogen, progesterone, and prolactin impact the number of terminal ending buds present during various stages of life)
-proliferation of connective tissue cells during wound healing

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13
Q

What is an examples of physiologic compensatory hyperplasia?

A

-regeneration of partially resected liver by the remaining hepatocytes (liver cells)

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14
Q

What is the typically cause of pathologic hyperplasia

A

-typically the result of excessive hormonal or growth factor stimulation

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15
Q

What can pathologic hyperplasia hyperplastic tissue lead to?

A

malignancy

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16
Q

What are example of pathological hyperplasia?

A

breast cancer, ovarian cancer, testicular cancer

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17
Q

Atrophy

A

shrinkage in the cell size by the loss of cell substance. No decrease in cell number. Leading to a decrease in the size of a tissue or organ

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18
Q

What are frequent causes of atrophy

A

-decreased workload
-loss of innervation (nerve growth in specific tissues or organs to regulate function)
-reduced blood supply
-inadequate nutrition
-aging (senile atrophy)

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19
Q

What can cause a decrease in cell size

A

-increased protein degradation
-reduced protein synthesis

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20
Q

Metaplasia

A

a reversible change in which one adult cell type is replaced by another adult cell type (mature somatic cell to mature somatic cell)

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21
Q

What is metaplasia a response to?

A

It is often a response to chronic irritation and inflammation that make cells better able to withstand stress

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22
Q

What are examples of metaplasia?

A

-in smokers (and vitamin A deficiency), ciliated columnar cells (ciliated columnar epithelial cels of the trachea and bronchi help clear foreign materials and mucous) are replaced by squamous epithelial cells, which are more rugged but not ciliated leading to coughing and increase in infections
-barretts esophagus
-intestinal metaplasia

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23
Q

Dysplasia

A

deranged cell growth of a specific tissue that results in cells that vary in size, number, shape, and organization (abnormal cell development and growth, mature to less mature)

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24
Q

What is dysplasia associated with?

A

chronic irritation and inflammation

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25
Q

When does dysplasia often occur?

A

often occurs in metaplastic squamous epithelium in the respiratory tract and uterine cervix

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26
Q

Is dysplasia adaptive?

A

Yes, in that it is potentially reversible after irritating cause has been removed (graded sequence after a certain point it is not reversible)

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27
Q

What is dysplasia a precursor of?

A

It is strongly implicated as a precursor (precancerous lesion) of cancer

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28
Q

What is an example of dysplasia?

A

Cervical dysplasia, which is a precursor for cervical cancer (HPV)

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29
Q

What causes dysplasia?

A

There can by many factors such as: development, mutation, or virus (HPV in cervical cancer)

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30
Q

Where tissue does dysplasia most often occur in?

A

epithelial tissue

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31
Q

Is metaplasia an adaptive process?

A

Yes, it is often triggered by environment (complicated by microorganism or inflammation)

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32
Q

What are the eight causes of cell injury?

A

-oxygen deprivation
-chemical agents
-infectious agents
-immunological reactions
-genetic defects
-physical agents
-nutritional imbalances
-aging

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33
Q

What are the general causes of oxygen deprivation?

A

hypoxia and ischemia

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34
Q

Hypoxia

A

oxygen deficiency

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35
Q

What are common causes of hypoxia?

A

-inadequate oxygenation of the blood (ex: pneumonia)
-reduction in the oxygen carrying capacity of the blood (ex: blood loss anemia or carbon monoxide poisoning in which CO forms a stable complex with hemoglobin that prevents oxygen binding)

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36
Q

Ischemia

A

loss of oxygenated blood supply to tissue

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37
Q

What are causes of ischemia

A

blockage or decrease in hearts ability to pump blood

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38
Q

What are examples of chemical agents?

A

poisons, air pollutants, CO, asbestos

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39
Q

What are examples of infectious agents

A

viruses, bacteria, fungi, parasites

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40
Q

what is an examples of immunological reactions

A

autoimmune disease

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41
Q

what are examples of genetic defects?

A

sickle cell anemia, familia hypercholesterolemia

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42
Q

What are examples of physical agents?

A

trauma, heat, cold, electric shock

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43
Q

Are nutritional imbalances a direct or indirect cause of injury?

A

typically indirect

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44
Q

What are examples of nutritional imbalances?

A

-nutritional deficiencies (caloric or vitamin)
-excess nutrition
-diabetes (can be caused by obesity, excess blood sugar levels can damage cells)
-atherosclerosis (can be caused by diet rich in fats, can result in blockage or coronary arteries)

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45
Q

How is aging a cause of cell injury?

A

As you age there is an accumulation of damage of reactive oxygen species, resulting in loss of telomerase function

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46
Q

What are characteristics of reversible injury?

A

cellular swelling or fatty change

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47
Q

cellular swelling

A

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

48
Q

Fatty change

A

occurs in hypoxic injury and various forms of toxic or metabolic injury, and is manifested by the appearance of small or large lipid vacuoles in the metabolism such as hepatocytes and myocardial cells

49
Q

What are characteristics of irreversible injury?

A

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

50
Q

What are mechanisms of cell injury?

A

-Free radical formation
-hypoxia/ ischemia
-increased intracellular calcium

51
Q

How does ATP depletion induce cell injury?

A

In the event of ischemia/hypoxia oxidative phosphorylation in the mitochondrion would decrease, resulting in a decrease in ATP production, this causes a decrease in NA+ pump action (allows for an influx in CA2+, H2O, K+, and Na+ resulting in swelling of the ER, swelling of cell, loss of microvilli, and blebbing), causes an increase in anaerobic glycolysis (results in less glycogen production, an increase in lactic acid, and an increase in pH which causes clumping of nuclear chromatin) as well as the detachment of ribosomes (results in decrease in protein synthesis)

52
Q

How does damage to mitochondria lead to cell injury?

A

An increase in cytosolic Ca2+, reactive oxygen species (oxygen stress) and lipid peroxidation leads to mitochondrial injury or dysfunction this results in a decrease in ATP production. In the event of apoptosis the weakening of the mitochondria membrane results in the leakage of cytochrome c (pre-apoptotic proteins) which triggers apoptosis. In the event of necrosis the weak membrane results in a permeability transition and an inability to generate ATP.

53
Q

How does an influx of calcium induce cell injury?

A

Cytosolic calcium concentration can increase due to release from intracellular stores or an influx across the plasma membrane. An increase leads to activation of various enzymes (ATPase, Phospholipase, Protease, and endonuclease)… The ATPase results in decreased ATP production, Phospholipase results in decrease phospholipids resulting in membrane damage, Protease results in a disruption of membrane and cytoskeletal proteins which also leads to membrane damage, and Endonuclease results in damage to nuclease chromatin

54
Q

How does increased oxidative stress induce cellular injury?

A

In the mitochondria the incomplete reduction of oxygen or inflmmation/radition/chemicals/reperfusion injury result in the production of a superoxide resulting in the production of a reactive oxygen species. The ROS can lead to the disruption of plasma membranes and organelles, loss of enzymatic activity and abnormal folding, and production of mutations and breaks in DNA…ROS can also be removed

55
Q

What are mechanisms of oxygen free radicals (OFRs) and reactive oxygen species (ROS)

A

-lipid peroxidation of membranes
-DNA fragmentation
-Protein oxidation and cross-linking (C & M residues)

56
Q

How does lipid peroxidation of membranes work?

A

The carbon carbon double bonds in the membranes are attacked, the membranes are then less hydrophobic, this then results in the conversion of lipids to detergents, ultimately leading to the reduction in membrane integrity

57
Q

How does DNA fragmentation work?

A

-Thymine peroxidation occur, so the base pairing between T and A is altered which leads to mis-substitution (mutation)
-single stranded DNA breaks can occur when there is breakage in the phosphodiester backbone resulting in reduced replication and transcription

58
Q

How does protein oxidation and cross linking work?

A

The protein oxidation results in altered protein structure, increased protein degradation, and loss of enzymatic activity

59
Q

What are cellular mechanisms that deal with OFRs and ROS?

A

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

60
Q

How doe antioxidants deal with OFRs and ROS?

A

they scavenge (react and neutralize) free radicals
-many are sold as dietary supplements (vitamin C and E, beta-carotene)

61
Q

How does sequestration of free ionized iron and copper deal with OFRs and ROS?

A

-free ionized iron and copper can cause ROS and OFRs via fenton reaction the use of treansferrin (Fe), ferritin (Fe), and ceruloplasmin (Cu) can sequester these metal ions to prevent them from causing ROS/OFR production

62
Q

How can defects in membrane permeability induce cell injury?

A
  • damage to the mitochondrial membrane results in decreased ATP production which leads to necrosis and apoptosis
    -damage to plasma membrane results in the loss of osmotic balance allowing for an influx of fluids and ions as well as cellular contents
    -damage to lysosomal membranes can result in the leakage of enzymes into the cytoplasm which can result in the activation of the acid hydrolases in the acidic intracellular pH of the injured cell
63
Q

apoptosis

A

a pathway of cell death that is induced by a tightly regulated suicide program in which cells destined to die activate enzymes capable of degrading the cells own nuclear DNA and cytoplasmic proteins

64
Q

What are physiological causes of apoptosis?

A

-programmed destruction of cells during embryogenesis
-involution of hormone-dependent tissues upon hormone deprivation: endometrial cell breakdown during the menstrual cycle
-cell loss in proliferating cell populations: intestinal crypt epithelia
-elimination of potentially harmful self-reactive lymphocytes: before or after their mutation
-cell death induced by cytotoxic T lymphocytes

65
Q

What are pathological causes of apoptosis?

A

-DNA damage
-accumulation of misfolded proteins
-cell injury in certain infection (viral infections)
-pathological atrophy in parenchymal organs after duct obstruction (pancreas, kidney, parotid gland)

66
Q

How does the Bcl-2 family effectors (Bax, Bak) trigger the mitochondria to release cytochrome c?

A

Once the Bcl-2 sensors receive a apoptotic signal the Bax or Bak effector attaches to the mitochondrial outer membrane and exposes the BH3 domain, this domain then dimerizes together with other effectors and oligerimization, creating a pore in the membrane which allows for the release of cytochrome c

67
Q

How does cytochrome c activate the initiator caspases?

A

When cytochrome c is release it binds with apaf-1, the binded protein then undergoes then binds with other bound apaf-1 to create a apoptosome, a procapase binds which triggers the conversion of an additional procaspase to the active form

68
Q

What role do Bcl-2 famil proteins play in apoptosis?

A
  • the Bax, Bak, and Bad proteins can increase mitochondrial membrane permeability by forming a dimer and inserting into the mitochondrial membranes (they are pro-apoptotic proteins)
    -Bcl-2 and Bcl-x can bind Bax family proteins and inhibit their function (they are anti-apoptic proteins)
69
Q

What happens when cytochrome is released?

A

When it is released it can activate caspase- 9 (initiator) to initiate the caspase cascade: caspases (cysteine-aspartic proteases, cysteine aspartases or cysteine aspartate-directed proteases)

70
Q

What are the two types of caspases?

A

-initiator (caspase 8 and 9)
-executioner (caspase-3 and 7)

71
Q

What can active caspases do?

A

-they can lead to the activation of other proteases, resulting in the degradation of cytoskeletal proteins
-they can lead to the activation of endonuclease, cleavage of DNA which leads to DNA fragmentation occurs (DNA ladder)

72
Q

How does the activated executioner caspase result in DNA fragmentation?

A

The caspase inactivates the inhibitor (iCAD/DFF45)of caspase activated DNase (CAD) which releases the active CAD/DFF40/CPAN (CAD is also called DNA fragment factor or caspase activate nuclease) the active CAD allows for the fragmentation of DNA in the nuclease during apoptosis (why lines can be seen)

73
Q

How do blebs occur?

A

Dying cells collapse into cytoplasmic buds and apoptotic bodies

74
Q

What happens to cells undergoing apoptosis?

A

The dead cells undergo phagocytosis through the use of macrophages.
-the macrophages clear the dead cells before they are able to release their cytoplasmic contents in order to prevent triggering an inflammatory response and prevent any remains of the dead cell from leaving

75
Q

What are intrinsic apoptosis sensor proteins?

A

-Bim
-Bid
-Bad (sensor, regulator, and effector)

76
Q

What are intrinsic apoptosis regulator proteins?

A

-BCL-2
-BCL-x

77
Q

What are intrinsic apoptosis effector proteins?

A

-Bax
-Bak

78
Q

What are extrinsic apoptosis proteins?

A

-Fas ligand (which binds to)
-TNF receptor

79
Q

What are intrinsic initiator caspases?

A

9 (turns on caspase 3)

80
Q

What are extrinsic initiator caspases?

A

8 (turns on caspase 3)

81
Q

What are executioner caspases?

A

3, 6, 7

82
Q

Physiology

A

-Mechanisms of how cells, tissues, organs, and our body work together. This can be at molecular, cellular, or the entire body level
-often reffering to the regulation or regulatory mechanisms under normal physiological (healthy) conditions

83
Q

Pathology

A

-Deals with the causes and processes of diseases
-refers to a disease state or abnormal state that may cause disease

84
Q

Uterus enlargement due to pregnancy is mainly caused by:
A. Commonly caused by atrophy and protein degradation
B. Hormone-induced hypertrophy of uterus smooth muscles
C. Hormone- induced hyperplasia of endometrium
D. Hormone-induced metaplasia of uterus smooth muscle cells
E. A and B

A

B Hormone-induced hypertrophy of the uterus smooth muscles

85
Q

What can increases the risk of breast cancer in women?

A

Hormone (excess estrogen)- induced hyperplasia in endometrium can be seen during menopause due to lower level of progesterone

86
Q

Uterus enlargement during pregnancy is mainly caused by? (ALT)
A. Estrogen-induced hyperplasia of the uterus smooth muscles
B. Estrogen-induced hypertrophy of uterus smooth muscle cells
C. Estrogen-induced activation of BCL apoptosis pathway in uterus smooth muscle cells
D. Estrogen-induced metaplasia of uterus smooth muscle cells
E. Testosterone-induced dysplasia of endometrial cells

A

B. Estrogen-induced hypertrophy of uterus smooth muscle cells
-Hypertrophy in smooth muscle cells is correct because although the uterine growth in the first few weeks of pregnancy is accompanied by increased numbers of smooth muscle cells (hyperplasia) the predominant growth of the uterus during pregnancy is stretching-induced enlargement of smooth muscle cells

87
Q

Which of the following may develop into cancer?
A. hyperplasia
B. Hypertrophy
C. Metaplasia
D. A and B
E. A and C

A

E. A and C
-hyperplasia and metaplasia can lead to pre-cancer lesions and often have similar causes
-if dysplasia was listed it would have also been considered a possibility to develop cancer as metaplasia is a change in cellular identity at stem cell level (epigenetic reprogramming) and is a precursor to low-grade dysplasia, which can culminate in high-grade dysplasia and carcinoma

88
Q

Hyperplasia is likely caused by?
A. increased work load
B. increased growth factors or hormone
C. chronic irritation
D. increased protein synthesis
E. All of the above

A

B. increased growth factors or hormone
- options A and D are associated with hypertrophy and C is associated with dysplasia and metaplasia

89
Q

The liver has a very high capacity to regenerate after surgical resection. This is caused by:
A. A significant increase in the cell size of remaining hepatocytes
B. A transdifferentiation of clotted platelets and other blood cells into hepatocytes
C. an increased proliferation of the remaining hepatocytes
D. A migration of regenerated hepatocytes in the bone marrow into the liver
E. none of the above

A

C. An increased proliferation of the remaining hepatocytes
-the liver has the capability to regenerate via cell proliferation, all others are considered confounding answers

90
Q

Barretts esophagus is the result of:
A. hypertrophy of the squamous epithelial cells in the lower part of the esophagus
B. Hyperplasia of the squamous epithelial cells in the lower part of the esophagus
C. Metaplasia of the squamous epithelial cells in the lower part of esophagus
D. atrophy of the squamous epithelial cells in the lower part of esophagus
E. A and B

A

C. metaplasia of the squamous epithelial cells in the lower part of esophagus
-this is due to metaplasia caused by chronic irritation by gastric acid (acid reflux)

91
Q

Identify the FALSE statement about dysplastic cells.
A. cells can have an increase in size
B. cells can have a decrease in size
C. cells in the tissue retain their normal organization (structure)
D. can be induced by chronic irritation
E. Dysplasia may lead to cancer

A

C. Cells in the tissue retain their normal organization

92
Q

T/F the hyperplasia associated with formation of terminal end buds (TEBs) and ductal elongation during puberty is a pathological process seen only in breast cancer

A

False- physiological breast development, hyperplasia can be physiological

93
Q

T/F during menopause, breast cancer may develop due to aberrant estrogen receptor activation

A

True- aberrant means “non normal”…progesterone levels drop and remove a brake on estrogen signaling which allows estrogen to overdrive cell proliferation

94
Q

T/F estrogen binding to its cytoplasmic receptor leads to activated estrogen receptor moving to the nucleus where it functions to enhance gene transcription

A

true

95
Q

T/F hyperplasia in the smooth muscle cells of the uterus is primarily responsible for uterine enlargement during pregnancy

A

false- hypertrophy in the uterus is associated with enlargement

96
Q

T/F hormone (excess estrogen) induced hyperplasia in endometrium occurs during menopause due to reduced progesterone signaling

A

True- hyperplasia occurs

97
Q

T/F dysplasia is characterized by abnormal changes in cell structure/number and can be a precursor to cancer

A

True- dysplastic cells can develop into cancer

98
Q

Which of the following is a characteristic of irreversible cell injury that is not associated with reversible cell injury?
A. cellular swelling
B. formation of lipid vacuoles in the cytoplasm
C. swelling of endoplasmic reticulum
D. disruption of plasma membrane
E. all of the above

A

D. disruption of plasma membrane
-loss of ATP generation and membrane integrity are characteristics of irreversible cell injury

99
Q

Calcium influx during cell injury can cause the following
A. activation of ATPase
B. activation of phospholipase
C. activation of protease
D. activation of endonuclease
E. all of the above

A

E. all of the above
-the activation of many enzymes associated with these functions is linked to calcium signaling

100
Q

ATP depletion can inhibit protein synthesis by the following mechanism
A. Na+ pump does not function
B. increased anaerobic glycolysis
C. mitochondria swellong
D. clumping of nuclear chromatin
E. detachment of ribosomes

A

E. detachment of ribosomes
-ribosomes are attached to ER, the place for protein synthesis. ATP depletion can cause dissociation of polysomes into monosomes and ribosome detachment from ER. You cannot have normal protein synthesis with these structural changes in the ER.

101
Q

T/F cellular swelling accompanies both reversible and irreversible cell injury

A

true

102
Q

T/F hypoxia is described as inadequate oxygenation of the body

A

true

103
Q

T/F myocardial cell death following an ischemic episode is visualized within minutes on light microscopy

A

false- the time-scale for visualizing cell death in the heart following ischemia is a couple hours for EM and several hours for light microscopy

104
Q

Increased oxidative stress often cause cell injury by the following mechanisms EXCEPT:
A. disruption of plasma membrane
B. Disruption of organelles
C. inactivation of some enzymes
D. induction of DNA damages
E. decreased protein degradation

A

E. decreased protein degradation
-protein oxidation (cross-linking) can increase protein misfolding and increase protein degradation

105
Q

The following may reduce oxygen free radicals and reactive oxygen species in cells EXCEPT:
A. superoxide dismutase (SOD)
B. Glutathione peroxidase
C. Catalase
D. Vitamin E
E. all of the above

A

E. all of the above

106
Q

Increased membrane permeability can be caused by the following:
A. phospholipid loss
B. lipid breakdown products
C. damage to cytoskeletal proteins
D. A and B
E. A, B, and C

A

E. A, B, and C

107
Q

The following sites of membrane damage are involved in cell injury EXCEPT?
A. mitochondrial membrane
B. plasma membrane
C. lysosomal membrane
D. ER membrane
E. all of the above

A

D. ER membrane
-losing ribosomes does not technically mean membrane damage, losing ribosomes damages ER function

108
Q

T/F free radical formation following cells following laser irradiation chemically reduces cell structures like lipids, proteins, and nucleic acids

A

False- oxidizes…ROS do not directly impact cell size

109
Q

T/F calcium overload is an injurious agent that can be inappropriately activate enzymes that damage cellular homeostasis

A

True

110
Q

Intrinsic apoptotic pathway may be activated by the following EXCEPT?
A. radiation-induced DNA damages
B. protein missfolding-induced ER stress
C. growth factor withdrawal
D. binding of Fas ligand to its receptor
E. all of the above

A

D. binding of the Fas ligand to its receptor
-Fas and TNF can activate extrinsic apoptotic pathway

111
Q

The role of cytochrome c in apoptosis is to:
A. increase mitochondrial membrane permeability
B. degrade Bcl-2
C. activate initiator caspases
D. phosphorylate and activate endonucleases
E. all of the above

A

C. activate initiator caspases
-works to form an apoptosome which can activate initiator caspases (procaspase 9)

112
Q

Which of the following molecules can increase mitochondrial membrane permeability?
A. Bcl-2
B. Bax/Bak
C. cytochrome c
D. TNF
E. caspase 3

A

B. Bax/Bak
-Bax, Bak, and Bad proteins can form dimers/oligomers and insert into mitochondrial membrane and increase membrane permeability so that cytochrome c can be released into the cytoplasm

113
Q

Which of the following statements about apoptosis and necrosis is TRUE?
A. apoptosis and necrosis can occur under both physiological and pathological conditions
B. cell size is enlarged when apoptosis and necrosis occurs
C. inflammation in surrounding cells and tissues can be seen when cells undergo apoptosis
D. DNA is fragmented into nucleosome size when necrosis occurs
E. none of the above

A

E. none of the above

114
Q

T/F unlike necrosis, apoptosis is never observed physiologically

A

False- necrosis is pathological cell death and there are many physiological examples of apoptosis

115
Q

T/F common pathological causes of apoptosis include DNA damage and accumulation of missfolded proteins

A

True

116
Q

T/F procaspase-3 binds cytochrome c to induce formation of the apoptosome

A

False- Apaf-1 binds cytochrome C and oligomerizes to form apoptosome to recruit procaspase 9

117
Q

In the event of ischemia in myochondrial cells when can damage and injury be observed?

A
  • non contractile after 1-2 minutes (reversible)
    -cell death occurs after 20-30 minutes
    -appear dead by electron microscopy at 2-3 hours
    -appear dead by light microscopy at 6-12 hours

Patho Exam 4 (6 decks)

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