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CMOD- Block1 > Path: Adaptation, Injury, Death (Part 3) > Flashcards

Path: Adaptation, Injury, Death (Part 3) Flashcards

1
Q

Define Infarction

A

Ischemic necrosis of an organ or tissue

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2
Q

Define necrosis

A

The appearance a dead organ or tissue takes on in a person who remains alive

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3
Q

Define autolysis

A

The morphology all of the organs and tissues take on when a person dies. (Differs from Necrosis)

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4
Q

Which of the two, autolysis or necrosis, elicits an acute inflammatory response?

A

Necrosis

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5
Q

How would you characterize autolysis on a cellular level?

A

gradual fading of the components of every cell, all at the same rate

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6
Q

What is the #1 cause of infarction to an organ or tissue?

A

occlusion of the vessel by thrombus or thromboembolus.

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7
Q

List the 4 factors that have influence on whether reversible ischemia becomes irreversible infarction.

A

1- Vulnerability of the tissue
2- rate of ischemic development
3- alternative blood supply
4- blood oxygenation

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8
Q

How quickly do ischemic neurons begin dying?

A

In as little as 4 minutes

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9
Q

How quickly do ischemic cardiac myocytes begin dying?

A

In as little as 20 mins

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10
Q

Slowly progressive ischemia gives the body time to grow ________________ into the ischemic area.

A

new collateral arteries

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11
Q

What is claudication?

A

The pain of ischemia

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12
Q

What is a positive effect of claudication?

A

It stimulates the body to undergo angiogenesis, to get around the ischemia, alleviating the disease.

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13
Q

Why in the case of the lungs, mesentery and liver, does ischemia less commonly lead to infarction?

A

Collateral blood supplies

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14
Q

Any disease that impairs blood oxygenation in the lungs or blood oxygen-carrying capacity, makes ischemia anywhere in the body more or less likely to cause infarction?

A

MORE

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15
Q

“White anemic” infarcts are typical of solid organs with ______ ________ circulation, such as the heart, the spleen and the kidneys.

A

End-arterial

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16
Q

“Red hemorrhagic” infarcts have several (3) different mechanisms. Name them.

A

1- venous occlusion
2- dual or anastomosing blood supply
3- reperfusion

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17
Q

Briefly describe red hemorrhagic infarcts.

A

When tissue infarcts, the blood vessels start breaking down and this causes hemorrhage into the dead tissue.

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18
Q

True or false: In many organs, infarcts tend to be central, capsular and circularly-shaped. If false, give correct description.

A

False.

Peripheral, subcapsular and wedge-shaped

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19
Q

If a cerebral artery is occluded, leading to ischemic necrosis, the cerebral infarction tends to develop ________ necrosis, that is the solid tissue turns to ______ and drains away.

A

Liquefactive necrosis; turns to liquid

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20
Q

Why does liquefaction occur in the brain following infarct/during necrosis?

A

Microglial cells transform into debris eating macrophages within a cerebral infarction and the cells that make collagen and convert infarcts in other organs into scars tend to be excluded by the blood-brain barrier (BBB).

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21
Q

Reperfusion can render a cerebral infarction ________ (bad).

A

hemorrhagic

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22
Q

Injury to cardiac myocytes sufficient to kill them causes the release of their _______ contents into the bloodstream in a characteristic temporal pattern.

A

Enzyme

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23
Q

_______ ___________ is an enzyme that catalyzes the transfer of phosphate from creatine phosphate to ADP, creating ATP.

A

Creatine phosphokinase (CPK) or creatine kinase for short

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24
Q

CPK is concentrated in what two organs in particular?

A

Brain and muscle

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25
Q

CPK is composed of ___ and ___ dimers.

A

M & B

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26
Q

The ____ fraction (dimer) of CPK is released into blood with myocardial necrosis.

A

MB

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27
Q

MB serum levels will be elevated beginning ___ hrs after an MI and peak around ____ hrs, falling back to normal around ____ hrs after the myocytes died.

A

3hrs; 24hrs; 48hrs

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28
Q

AST serum levels will be elevated ___ hrs after MI, peak around ____ hrs and normalize around ___ days.

A

24hrs; 48hrs; 4 days

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29
Q

Following an MI, LDH serum levels will be elevated at ___ hrs, peak around ___ hrs and normalize around ___ days.

A

24hrs, 72hrs, 7 days

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30
Q

_______ are proteins that regulate calcium-mediated contraction of cardiac and skeletal muscle.

A

Troponins

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31
Q

What are the cardiac-specific versions of the Troponins?

A

Troponin-I and Troponin-T

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32
Q

Following an MI, cardiac troponins will be elevated after about ___ hrs, peaking around ___ hrs but not normalizing until around ___ days.

A

3hrs; 24hrs; 10 days

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33
Q

True or false: the sensitivity for MI of CK-MB and Troponin assays are both above 50%.

A

False, they are both at 35%

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34
Q

True or false: the specificity for MI of CK-MB and troponin assays are both over 90%.

A

False. 80% for CK-MB and 96% for troponin

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35
Q

The sensitivity of the troponin level for the Dx of acute MI improves to 90% if it is assayed ___ hrs after the onset of chest pain.

A

10 hrs

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36
Q

Why is it recommended to repeat troponin assay at least once 3-6 hrs after the initial level?

A

To rule in or out the Dx of acute MI, a second assay of troponin levels is recommended approx 10 hrs after the MI because of the increased (90%) sensitivity of the assay after 10 hrs.

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37
Q

For the Dx of acute MI, an elevated troponin needs to be combined with at least one of the following:

A

1- symptoms of ischemia
2- EKG evidence of ischemia
3- imaging evidence of ischemia
4- ID of an intracoronary thrombus by angiography or autopsy.

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38
Q

True or false: Highly sensitive troponin assays are very specific for the Dx of acute MI.

A

False. Highly sensitive troponin assays are POORLY specific for the Dx of acute MI, illustrating the inevitable tradeoff between sensitivity and specificity, and making it important to combine a positive test with other evidence of acute MI to make this Dx.

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39
Q

Gangrene is a distinctive form of ischemic necrosis characterized by _______ and ______, typically of distal extremity, but also sometimes of internal organs.

A

blackening and shrinkage

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40
Q

True or false: gangrene is primarily a term for micro-pathology.

A

False. Gross pathology

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41
Q

Treatment of gangrene is surgical or non-surgical?

A

Surgical. Amputation or excision of the affected tissue/organ.

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42
Q

______ necrosis is a distinctive form of necrosis grossly resembling cheeese, associated with TB, histoplasmosis and similar diseases.

A

Caseous necrosis

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43
Q

Caseous necrosis is a term describing gross or micro pathology?

A

Gross

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44
Q

Caseating necrosis is usually caused by ______ infections or infections caused by bacteria resembling ______.

A

Fungal; fungi (mycobacteria [Mycobacterium tuberculosis])

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45
Q

True or false: Mycobacteria and most fungi are fast growing and usually sensitive to the same abx used to treat acute bacterial infections.

A

False. Slow growing and are sensitive to different abx than the ones used to treat acute bacterial infections.

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46
Q

T/F: Ischemia leads to liquefication in tissues other than brain tissue.

A

False

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47
Q

What is an abscess?

A

A localized area of liquefactive necrosis.

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48
Q

______ infections are the most common cause of abscesses.

A

Necrotizing infections

49
Q

The usual treatment for an abscess is ______.

A

Drainage

50
Q

Fat necrosis is the form of tissue death when fat digested by ________ _______, releases fatty acids, which bind calcium, creating a chalky white soap-like material (saponification).

A

pancreatic lipase

51
Q

What determines treatment for necrosis?

A

The type of necrosis. I.e. gangrenous (surgery), caseous (antifungals), abcesses (drainage).

52
Q

________ is the condensation, shrinkage and hyperbasophilia of a dead cell nucleus seen in apoptosis and sometimes necrosis.

A

Pyknosis

53
Q

__________ is the fragmentation of a pyknotic, dead nucleus, seen in both necrosis and apoptosis.

A

Karyorrhexis

54
Q

Karyolysis is:

A

The fading away of a dead nucleus

55
Q

_______ _________ is a term for the microscopic pathology of the most common form of necrosis because it makes the dead cell look like a tiny condensed fibrin blood clot.

A

Coagulative necrosis.

56
Q

Coagulative necrosis causes the cytoplasm to be a denser pink (eosinophilic or basophilic?) with condensed, denatured proteins.

A

eosinophilic

57
Q

Do cells that have died of ischemia show it immediately?

A

No. Coagulative necrosis of cardiac myocytes: 4-12 hrs. Neurons: 12-24 hrs.

58
Q

________ is a pathway of cell death induced by a tightly regulated intracellular program of activating enzymes that degrade the cell’s own DNA and proteins.

A

Apoptosis

59
Q

Physiologic or pathologic apoptosis occurs in embryogenesis, involution (uterine transformation from pregnant to non-pregnant state), ending inflammation and negative selection of self-reactive lymphocytes?

A

Physiologic apoptosis

60
Q

Physiologic or pathologic apoptosis occurs in injury due to hypoxia, heat, radiation or chemotherapy, certain viral diseases, duct obstruction, transplant rejections and tumors?

A

Pathologic

61
Q

What are caspases?

A

The enzymes that orchestrate and carry out apoptosis.

62
Q

What is the family of proteins that regulates apoptosis?

A

BCL2 family.

63
Q

Is the BCL2 family of proteins pro or anti-apoptotic?

A

Both

64
Q

Name the 3 principal members of the BCL2 family that are anti-apoptotic.

A

BCL2, BCL-XL and MCL1

65
Q

Two pro-apoptotic members of the BCL2 family, _____ and _______ oligomerize in the outer membrane of mitochondria, if activated, and promote permeability of the mitochondrial outer membrane.

A

BAX and BAK

66
Q

List the 5 members of the BCL2 family of proteins that serve as sensors of cell injury and determine, whether the pro or anti-apoptotic members of the family rule the cell.

A

BAD, BIM, BID, Puma and Noxa

67
Q

The _________ apoptotic pathway starts with increased mitochondrial permeability releasing pro-apoptotic molecules, especially _______ __ , into the cytoplasm from the intermembrane space of the mitochondria.

A

Intrinsic; cytochrome c

68
Q

In apoptosis, cytochrome c binds to __________, which forms a wheel-like structure called the _________.

A

apoptosis-activating factor-1 (APAF-1); apoptosome

69
Q

In apoptosis, the apoptosome binds _______ (initiator caspase), which activates nearby caspase-9 molecules and initiates a cascade of activation of various caspases, culminating in the activation of __________ and _________ (executioner caspases.)

A

Caspase-9; Caspase-3; Caspase-6

70
Q

What do executioner caspases do?

A

Deactivate an inhibitor of cytoplasmic DNase and promote fragmentation of the nucleus, releasing DNA to this DNase.

71
Q

The _______ (death receptor) pathway of apoptosis begins with binding of tumor necrosis factor (TNF) to a ________________ or binding of a protein celled Fas ligand (FasL) to a cell surface receptor named Fas.

A

extrinsic; cell surface type 1 receptor (TNFR1)

72
Q

The binding of FasL to Fas causes 3 or more attached Fas-associated death domains (FADDs) to activate _________ and ________, initiating a cascade of activating various caspases, with the same culmination as the intrinsic pathway.

A

Caspase-8; caspase-10

73
Q

The protein called FLIP, found in some cells, binds to pro-caspase-8 and prevents it from what?

A

initiating the caspase cascade of apoptosis.

74
Q

How can FLIP be used against a cell by a virus?

A

The virus can use FLIP to block apoptosis of cells they have infected so they have time to replicate within the cell before it dies.

75
Q

Do cells maintain an intact membrane in apoptosis?

A

Yes.

76
Q

Do cells maintain an intact membrane in necrosis?

A

No.

77
Q

Apoptosis causes __________ normally present on the inner side of the cell membrane to flip to the outside, making the cell a target for _________.

A

phosphatidylserine; phagocytosis

78
Q

Is there an acute inflammatory (neutrophilic) response in apoptosis?

A

No.

79
Q

Define necroptosis.

A

pathway of cell death that starts out like apoptosis and ends up like necrosis

80
Q

Necroptosis starts out with cell surface binding of ___ or ___.

A

TNF or FasL

81
Q

The necroptosis pathway goes through ___ ___ ___ _ and _, which are known by the acronyms ___ and ___.

A

receptor associated kinase 1 and 3; abbreviated RIP1 and RIP3

82
Q

RIP1 and RIP3 initiate breakdown of the ____ membrane, which releases ___ ___ ___ and general destruction resembling _____.

A
  • lysosomal membrane
  • reactive oxygen species
  • necrosis
83
Q

What are two synonyms for necroptosis?

A
  1. Programmed necrosis

2. Caspace-independent programmed cell death

84
Q

Give examples of each: physiologic and pathologic necroptosis

A

Physiologic: normal bone growth
Pathologic: reperfusion injury, acute pancreatitis, steatohepatitis, neurodegenerative disease

85
Q

What is another name for the enzyme Caspace-1, and what is its function?

A

Interleukin-1beta converting enzyme; it cleaves a precursor of interleukin-1beta to its active form; acts in the pyroptosis pathway

86
Q

Caspace-1 and Caspace-11 induce cell death manifested by ___ ____ and release of ____.

A

cell swelling and release of interleukin-1beta

87
Q

True or false: the release of interleukin-1beta elicits a neutrophilic response.

A

True.

88
Q

How is pyroptosis similar to apoptosis, and how is it similar to necroptosis?

A

Like apoptosis pyroptosis is caspace-mediate.

Like necroptosis, pyroptosis has a neutrophilic inflammatory response.

89
Q

What is pyroptosis?

A

the cell-death pathway initiated by innate immune system receptors that activate the multi-protein inflammasome; mediated by caspace-1 and caspace-11, which result in release of interleukin-1beta for a neutrophilic response and fever (hence “pyro-“)

90
Q

____ salts are sometimes deposited at sites of tissue injury or necrosis.

A

Calcium

91
Q

What is dystrophic calcification?

A

calcium salt deposits at sites of necrosis accompanied by small amounts of iron, magnesium, or other minerals

92
Q

What are the areas of necrosis in which dystrophic calcification occurs?

A

coagulative, caseous, liquefactive, and especially fat necrosis

93
Q

What is Monckenberg’s medial calcific sclerosis?

A

condition in which the internal elastic lamina of arteries calcifies independently of atherosclerosis, and the calcification can spread to involve the tunica media

94
Q

What is the role of calcification in atherosclerosis?

A

it is a common complication that causes the blood vessels to lose elasticity and the ability to constrict and dilate in response to physiologic needs

95
Q

Atherosclerosis is a disease of which tissue layer of the arteries?

A

tunica intima

96
Q

Stiffening of the arteries (due to any condition) makes them less elastic. What effect does this have on blood pressure?

A

this requires a higher systolic bp to maintain adequate flow since the arteries can’t squeeze out blood as well in diastole (when the heart is filling and not pumping)

97
Q

Gross calcifications appear ___ while microscopically (histologically) they appear ___.

A

white and chalky; basophilic (blue)

98
Q

Single necrotic cells that calcify and then layers of further calcification can create a ____ ____.

A

psammoma body

99
Q

Psammoma bodies are features of papillary carcinoma of the ___ and ___, as well as ____.

A

thyroid and ovary, as well as meningiomas

100
Q

What are ferriginous bodies?

A

asbestos fibers that have had their pointed ends coated by iron and calcium salt deposits;

101
Q

Ferriginous bodies that go on to form bone are called what?

A

heterotropic bone formation

102
Q

What are 4 common causes of hypercalcemia?

A
  1. hyperparathyroidism
  2. bone resorption
  3. vitamin D disorders
  4. renal failure
103
Q

Does PTH raise or lower levels of calcium in the blood?

A

raise

104
Q

What’s the risk of a parathyroid tumor?

A

it can secrete large amounts of PTH which would raise blood calcium levels, leading to hypercalcemia

105
Q

Tumors of bone marrow can cause a high level of bone ____.

A

resorption

106
Q

What is the relationship between Williams syndrome and vitamin D?

A

patients with Williams syndrome have an abnormal sensitivity to vitamin D

107
Q

How does renal failure contribute to hypercalcemia?

A

renal failure causes phosphate retention and secondary hyperparathyroidism

108
Q

What are the top 6 most common chief complaints?

A
  1. Abdominal pain
  2. Chest pain
  3. Dyspnea
  4. Fatigue
  5. Fever
  6. Syncope
109
Q

Describe dry gangrene.

A

Dry gangrene begins at the distal part of the limb due to ischemia. Dry gangrene is mainly due to arterial occlusion. There is limited putrefaction and bacteria fail to survive. Dry gangrene spreads slowly through portions of tissue where the blood supply is inadequate to keep tissue viable. The affected part is dry, shrunken and dark reddish-black, resembling mummified flesh.

110
Q

Describe wet gangrene.

A

This condition is characterized by thriving bacteria and has a poor prognosis (compared to dry gangrene) due to septicemia resulting from the free communication between infected fluid and circulatory fluid. The affected part is edematous, soft, putrid, rotten and dark.

111
Q

Apoptosis is energy dependent or independent?

A

Dependent

112
Q

microscopically, an apoptotic cell shrinks or expands and is seen to be basophilic or eosinophilic?

A

shrinks and is eosinophilic

113
Q

What exactly does BCL2 do to regulate the efflux of Cytochrome C from the inner matrix of the mitochondria?

A

Stabilizes the mitochondrial membrane. If BCL2 is knocked out, Cyt C will efflux from the mitochondrion, into the cytoplasm and initiate apoptosis.

114
Q

List the toxic oxygen products of oxidative phosphorylation, in order that they occur beginning with O2 and ending with H2O

A

O2»>O2(-)»>H2O2»>(-)OH»>H2O

Molecular oxygen»>Superoxide»>Hydrogen peroxide»>Hydroxyl ion (most destructive)»>Water (delicious)

115
Q

What enzyme catalyzes the conversion of O2&raquo_space;> O2-?

A

NADPH Oxidase (Oxidizes NADPH, reduces O2)

116
Q

In what ways, on a molecular level, do free radicals damage cells?

A

1- Peroxidize lipids (damage cell membrane)

2- Oxidation of DNA & proteins (oncogenesis)

117
Q

What are 3 ways the body eliminates oxygen free radicals?

A

1- Antioxidants
2- Enzymes [Superoxide dismutase (O2-), Glutathione peroxidase (-OH), catalase (H2O2)]
3- Metal carriers (ferritin for Fe2+, ceruloplasmin for Cu2+)

118
Q

List 2 methods of free radical injury that do not involve products of ox-phos.

A

1) CCl4- carbon tetrachloride (in cleaning agents) becomes CCl3- via CYP450 in liver and causes fatty liver disease. MOA: CCl3- causes irreversible membrane damage»>cell swells»>ER swells»>ribosomes pop off ER»>protein synthesis inhibited»>lysosomal enzymes not produced»>FAs build up in cell lysosomes bc not degraded= fatty liver disease.
2) reperfusion injury

119
Q

What is the hallmark of irreversible cell injury?

A

Damage to cell membrane

CMOD- Block1 (36 decks)

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