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BMS 460 > Lesson #10 - Exam 2 > Flashcards

Lesson #10 - Exam 2 Flashcards

1
Q

Cell injury will ensure following what?

A

disruption of homeostatic cellular mechanisms.

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2
Q

How does Ca++ overload cause cell injury?

A

Increased calcium causes dysfunction of:
1. ATPase - Decreased ATP production.
2. Phospholipase - Decreased production of phospholipids.
3. Protease - Causes disruption of membrane and cytoskeletal proteins.
4. Endonuclease - Causes nuclear chromatin damage.

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3
Q

When there is a lot more calcium in the cytosol compared to the extracellular matrix, ____________________ will occur.

A

Dystrophic calcification.

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4
Q

Two ways to maintain the calcium concentration gradient:

A
  1. Passive impermeability to calcium ions.
  2. The ATP-dependant active extrusion of calcium ions out of the cell.
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5
Q

True or false: Microscopic deposition of calcium salts will cause reversible cell injury .

A

FALSE - MACROscopic deposition of calcium salts will cause lethal cell injury and calcification of structures.

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6
Q

___________ is seen in chronic renal failure, which has depositions in the eye, heart, and blood vessels.

A

Calcification.

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7
Q

__________ is a medical condition that results from a previous disease.

A

Sequale.

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8
Q

Reversible injury:

A

Goes back to normal.

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9
Q

Irreversible injury:

A

Severe. Causes necrosis, apoptosis, and pyroptosis.

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10
Q

Persistent but sub-lethal injury:

A

Causes functional cell adaptations.

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11
Q

____________________: injury to the cell caused by a persistent stress, that can be relieved by functional changes.

A

Cellular adaptations.

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12
Q

Hypertrophy:

A
  1. A cellular adaptation.
  2. Causes increased cell size.
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13
Q

Hyperplasia:

A
  1. A cellular adaptation.
  2. Causes increased cell number.
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14
Q

Atrophy:

A
  1. A cellular adaptation.
  2. Causes decreased cell size.
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15
Q

Metaplasia:

A
  1. Cellular adaptation.
  2. Changes one cell to a different type of cell.
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16
Q

Dysplasia

A
  1. Cellular adaptation.
  2. Disorderly cell growth.
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17
Q

True or false: All cellular adaptations are benefitting the cell.

A

FALSE - Some cellular adaptations can be harmful to the cell.

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18
Q

Examples of harmful cellular adaptations:

A
  1. Dysplasia can transform CIS cells into precancerous lesions.
  2. Hypertrophy of cardiac muscles due to increased workload.
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19
Q

Timescale to sequale injury:

A
  1. ATP depletion.
  2. Biochemical dysfunction.
  3. Early ultrastructural changes.
    (All steps above this are reversible injury)
  4. Late ultrastructural changes.
  5. Early light microscopic changes.
  6. Late light microscopic changes.
    (Second half is when injury becomes irreversible
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20
Q

In _____________, pathological changes may be minimal or absent, due to a fast timescale not allowing full pathological mechanisms.

A

Acute injury.

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21
Q

Typical pathological findings 15 minutes after injury:

A
  1. Endoplasmic reticulum swelling and ribosome dislocation.
  2. Membrane rupture.
  3. Mitochondrial inclusions.
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22
Q

Typical pathological findings 4-8 hours after injury:

A
  1. Hypereosionphillia of the cytoplasm.
  2. Karolysis.
  3. Coagulative necrosis.
  4. Influx of neutrophils.
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23
Q

__________________ presents as leakage of pro-apoptotic proteins. Causing decreased ATP production, resulting in downstream effects.

A

Mitochondrial damage.

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24
Q

________ of ________, causes increased mitochondrial permeability, and activation of many cellular enzymes.

A

Entry of calcium.

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25
Q

Increased _______ ________ ________, causes damage to lipids, proteins, and DNA.

A

Reactive oxygen species.

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26
Q

________ ________ causes loss of cellular components when affecting the lipid bilayer, and enzymatic digestion of cellular components when affecting the lysosome.

A

Membrane damage.

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27
Q

________ _________ is caused by damaged DNA, and results in the activation of pro-apoptotic proteins.

A

Protein misfolding.

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28
Q

ATP-dependant Na+-K+ pump disruption:

A
  1. Causes cell swelling, due to Na+ and H2O moving into the cell (Hydropic/vacuolar degeneration)
  2. Mitochondrial swelling leads to decreased ATP production.
  3. Cell reverts to anaerobic glycolysis, so pH becomes acidic (lowers)
  4. Organelles break and disintegrate.
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29
Q

True or false: Myelin figures are clumps of nuclear chromatin.

A

FALSE - Myelin figures are rolled up phospholipid bilayers.

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30
Q

1st manifestation of almost all forms of cell injury:

A

Cellular swelling.

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31
Q

Decreased protein synthesis causes accumulation of _______ ______, contributing to a free fatty acid pool via _______________.

A
  1. Amino acids.
  2. Gluconeogenesis.
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32
Q

In hypoxic conditions what will provide energy? What will result from this?

A

In hypoxic conditions fatty acids will be broken down to provide energy, resulting in more lipid synthesis and accumulation.

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33
Q

_______ is a decrease in blood supply to an organ, tissue, or part caused by constriction of a blood vessel.

A

Ischemia.

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34
Q

Ischemia can result in -

A

Hypoxia of the cell.

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35
Q

Accumulations in normal tissues -

A

Excess fats - such as in a fatty liver.

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36
Q

Accumulation of abnormal substances -

A

It can occur because of faulty synthesis, metabolism, or transport.

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37
Q

Two examples of abnormal substance accumulation:

A
  1. Mutations causing defective folding of and transport of proteins.
  2. Deficiency of enzymes for lysosomal degradation.
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38
Q

List of pigments and phagocytosed particles that will accumulate -

A

Melanin, hemosiderin, bilirubin, inorganics.

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39
Q

Alcoholic fatty liver disease will occur due to -

A

Accumulation of fats, due to abnormalities in toxin metabolism.

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40
Q

Accumulation of endogenous materials occurring due to a lack of enzymes or transport proteins occurs in what condition:

A

Neimann-Pick C disease

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41
Q

Accumulations of exogenous materials, gained by ingestion of indigestible materials, is an example of -

A

Silicone dust inhalation.

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42
Q

True or false: alpha-antitrypsin is a major inhibitor of proteases, that are normally released from neutrophils at the site of inflammation.

A

TRUE.

43
Q

Deficiency of AAT:

A
  1. Autosomal recessive disorder.
  2. Gene SERPINA1 will impair the secretion of AAT from hepatocytes into serum.
  3. Causes liver disease in infants/children/adults.
  4. Causes lung disease in adults.
44
Q

Most common cause of cirrhosis of the liver in children:

A

Accumulation of AAT in heaptocytes.

45
Q

________________ increases the risk for hepatocellular carcinoma.

A

Anti-alpha-trypsin deficiency.

46
Q

AAT globules will be seen with which stain:

A

Periodic acid schiff reagent - PAS.

47
Q

True or false: AAT alleles are inherited codominantly, causing several forms and degrees of AAT deficiency.

A

TRUE!

48
Q

AAT alleles:

A
  1. M allele - normal.
  2. Z/S alleles - Deficient.
49
Q

Variants of AAT deficiency present a selective defect in the migration of ____ from the _____________ to the __________________.

A
  1. AAT
  2. Endoplasmic reticulum.
  3. Golgi apparatus
50
Q

Lung disease in adults is a symptom of -

A

AAT deficiency.

51
Q

What is the function of alpha-antitrypsin (AAT)?

A

To protect the lungs from proteases, that will normally be released at the site of inflammation.

52
Q

True or false: The neutrophil elastase is a powerful protease that will disrupt muscle tissue.

A

FALSE - Elastase is a powerful protease that will disrupt connective tissue.

53
Q

AAT levels below ____% will result in emphysema and liver disease, due to a lack of inhibition of proteases.

A

15%

54
Q

Panacinar emphysema:

A
  1. Respiratory bronchioles, alveolar ducts, and alveoli are destroyed by proteases.
  2. Primarily by elastases - that will destroy elastic fibers.
55
Q

What condition will occur due to a carcinogen inducing alveolar macrophages to secrete proteases, and chemoattractants to attract more neutrophils?

A

Smokers lung.

56
Q

This will cause a chronic release of elastase in the lungs, that bombards normal AAT levels without an AAT deficiency, causing emphysema -

a. Smokers lung.
b. Panacinar emphysema.

A

A - Smokers lung.

57
Q

________ is an irreversible cell injury that is a pathological consequence of cell injury and inflammation.

A

Necrosis.

58
Q

In necrosis, the first process where the mitochondria and RER swell, causing nuclear clumping and ruptured cell membranes, is called -

a. Karyorrhexis.
b. Pyknosis.

A

B - Pyknosis

59
Q

__________ is the step of necrosis where there are nuclear fragments and neutrophil interaction, causing cell death.

A

karyorrhexis.

60
Q

True or false: Necrosis is the death of a group of cells due to exogenous injury.

A

TRUE.

61
Q

Apoptosis steps:

A
  1. Cell must have the programmed suicide gene before beginning.
  2. A signal occurs to trigger apoptosis
  3. Nuclear changes occur, along with cytoplasmic fragmentation creating apoptotic bodies.
  4. Apoptotic bodies will be engulfed by macrophages to dispose of them.
62
Q

This irreversible cell injury occurs to a single cell:
a. Pyroptosis.
b. Apoptosis.
c. Necrosis.

A

B - Apoptosis.

63
Q

__________ is an inflammatory form of cell death caused various pathological stimuli, such as stroke/heart attack/cancer.

A

Pyroptosis.

64
Q

This is a proinflammatory programmed cell death that controls microbial infections.

a. Pyroptosis.
b. Necrosis.
c. Apoptosis.

A

A - pyroptosis.

65
Q

Mechanism of pyroptosis:

A
  1. Causes a release of pathogen-associated molecular patterns (PAMPs) and cytokines that activate pro-inflammatory immune cell mediators.
  2. Has early loss of plasma membrane integrity and shedding of membrane vesicles - similar to necrosis.
66
Q

The events of apoptosis in order:

A
  1. A trigger initiates apoptosis.
  2. Regulatory proteins will inhibit or promote the activation of caspases.
  3. Caspase activation will begin the process of cellular degradation.
  4. Apoptotic cell fragments are internalized by phagocytic cells.
67
Q

What regulatory proteins will inhibit the activation of caspases, which will promote it?

A

Inhibit = BCL-2, BCL-Xl, and others.

Promotes = BAX, BAD.

68
Q

What triggers the apoptotic cell fragments to be internalized by a phagocytic cell?

A

Ligands on the apoptotic cell go to the receptors on the phagocytic cell.

69
Q

________________ is the process by which dying or dead cells are removed by phagocytic cells.

A

Efferocytosis.

70
Q

True or false: In a macrophage mitochondria will interact with the endoplasmic reticulum to isolate lots of calcium in those organelles.

A

TRUE!

71
Q

When a ____________ encounters a dead cell, its mitochondria/ER will break up into smaller components to release ______ to break down the cell.

A
  1. Macrophage.
  2. Ca++
72
Q

_______________________________ is when a single macrophage ingests multiple dead cells.

a. High-stress apoptosis.
b. High-burden efferocytosis.
c. Low-burden karyocytosis.
d. High-stress efferocytosis.

A

B - High-burden efferocytosis.

73
Q

What is the purpose of high-burden efferocytosis?

A

To prevent tissues from dying and getting inflammation.

74
Q

What autoimmune diseases can form due to defects in efferocytosis:

A
  1. Chronic lung disease.
  2. Neurodegenerative disease.
  3. atherosclerosis.
75
Q

4 types of necrosis:

A
  1. Coagulative necrosis.
  2. Liquefactive necrosis.
  3. Fat necrosis.
  4. Caseous necrosis.
76
Q

In coagulative necrosis, ischemic cell injury leads to:

A
  1. Loss of the plasma membranes’ ability to maintain an electrochemical gradient.
  2. Influx of calcium ions and dysfunction of the mitochondria.
  3. Degradation of plasma membrane and nuclear structures.
77
Q

In _____________ necrosis, the tissue architecture is preserved for weeks due to rapid inactivation of cellular hydrolytic enzymes.

A

Coaugulative.

78
Q

Mechanism of liquefactive necrosis:

A
  1. Dead cells make the pH acidic,
  2. Acidic pH activates lysosomal enzymes.
  3. Results in liquefaction (making tissue fluid)
79
Q

Which form of necrosis will occur mostly in the brain, and may result in an abscess or cyst formation.

a. Coaugulative necrosis.
b. Liquefactive necrosis.
c. Fat necrosis.
d. Caseous necrosis.

A

b - liquefactive necrosis.

80
Q

True or false: Liquefactive necrosis causes the death of adipose tissue, resulting from trauma or pancreatitis.

A

FALSE.

Liquefactive necrosis by dead cells increasing the pH, and activating lysosomal enzymes.

Fat necrosis is caused by the death of adipose tissue, resulting from trauma or pancreatitis.

81
Q

Secondary liquefactive necrosis:

A
  1. Initially shows as coaugulative necrosis.
  2. Liquefy WBCs that invade necrotic tissue and release lytic enzymes.
82
Q

__________ necrosis is caused by death of adipose tissue due to trauma or pancreatitis, causing a release of digestive enzymes.

A

Fat

83
Q

_________ necrosis is a characteristic of lung tissue damaged by tuberculosis.

A

caseous necrosis.

84
Q

Gangrene is cellular death involving a _______ area, regardless of _______.

A
  1. Large area.
  2. Causation.
85
Q

Dry gangrene:

A
  1. Is a form of coagulative necrosis.
  2. Presents as dry, blackened, wrinkled tissue.
  3. Separated from healthy tissue.
86
Q

Wet gangrene:

A
  1. Form of liquefactive necrosis.
  2. Typically found in internal organs.
  3. Appears cold and black, foul smelling due to bacteria invasion.
87
Q

____________ is an interruption flow, that may cause hypoxia.

A

Ischemia.

88
Q

When a large area experiences ischemia causing necrotic tissue, it is called __________.

A

Infarction.

89
Q

When an infarction affects solid organs effectively turning them white, and its occlusion is composed of platelets, it is called -

a. white infarction.
b. red infarction.

A

a. white infarction

90
Q

When an infarction typically effects the lungs, and it’s occlusion is composed RBCs and fibrin strands, it is called -

a. white infarction.
b. red infarction.

A

b. red infarction.

91
Q

___________ ___________ is when a segment of the guts gets twisted on its mesentery, and the entire segment becomes dilated/gangrenous/hemorrhagic.

A

Intestinal volvulus.

92
Q

Intestinal volvulus is an example of:

A

ischemia-induced cell injury.

93
Q

Explain the mechanism by which ischemia activates neutrophils:

A
  1. Decreased O2 to the mitochondria a stop in ATP production, causing failure of the ATP dependant Na+, K+, and Ca++ pumps.
  2. Calcium overload causes changes in the metabolism of the bilayer and cytoskeletal damage, causing inflammation.
  3. Inducing adhesion and activate neutrophils.
94
Q

Activated neutrophils release:

A

activated O2 species, resulting in more free radicals through reperfusion.

95
Q

True or false: Ischemia causes catabolism of ATP, GTP, and nucleic acids, resulting in a swollen cell.

A

TRUE.

96
Q

True or false: Ischemia causes an enzyme conversion from xanthine oxidase to xanthine dehydrogenase.

A

FALSE - Ischemia causes an enzyme conversion of xanthine dehydrogenase to xanthine oxidase.

97
Q

Reperfusion is ____________ of blood flow, and forms ____ acid.

A
  1. restoration of blood flow.
  2. Uric acid.
98
Q

Toxic activated oxygen species are primarily caused by -

A

Reperfusion.

99
Q

Myocardial infarction will cause:

A

Heart attack.

100
Q

In normal cardiac tissue, there is __________ ________ in the sarcoplasm. That will catalyze the transfer of a phosphate from ________ _______ to ____.

A
  1. Creatine kinase.
  2. Creatine phosphate.
  3. ADP.
101
Q

Myocardial ischemia caused by occlusion of the coronary arteries will -

A

Cause necrosis within in 24 hours.
2. Have an eosinophillic cytoplasm, lacking striations.
3. Neclei will be pykonotic and irregularly shaped.

102
Q

Which creatine kinase type is mostly found in the lungs and brain?
a. CK-MM
b. CK-BB
c. CK-MB

A

b. CK-BB

103
Q

Which creatine kinase type is mostly found in the skeletal muscle and heart?
a. CK-MM
b. CK-BB
c. CK-MB

A

a. CK-MM

104
Q

Which creatine kinase type is mostly found in the myocardium?
a. CK-MM
b. CK-BB
c. CK-MB

A

c. CK-MB.

BMS 460 (13 decks)

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