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Pathoma > Chapter 1 - Growth Adaptations, Cellular Injury, and Cell Death > Flashcards

Chapter 1 - Growth Adaptations, Cellular Injury, and Cell Death Flashcards

1
Q

Hyperplasia and hypertorphy generally occur together. What is the exception to this rule?

A

Permanent Tissues

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2
Q

What are the 3 Types of Permanent Tissues?

A
  1. Cardiac Muscle 2. Skeletal Muscle 3. Nerves
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3
Q

Atrophy consists of what 2 mechanisms?

A
  1. Decrease in cell size 2. Decrease in cell number
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4
Q

The decrease in cell size in atrophy occurs via what mechanisms?

A
  1. ubiquitin-proteosome degradation of the cytoskeleton 2. autophagy of cellular components
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5
Q

In Barrett Esophagus, the nonkeratinizing squamous epithelium changes to what?

A
  1. Nonciliated 2. Mucin Producing 3. Columnar
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6
Q

Is Metaplasia reversible?

A

Yes, if the driving stressor is removed

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7
Q

What happens to metaplasia under persistent stress?

A

It progresses to dysplasia

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8
Q

What happens to dysplasia under persistent stress?

A

It progresses to carcinoma

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9
Q

What causes Keratomalacia?

A

Vitamin A deficiency

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10
Q

What is Keratomalacia?

A

Conjuctiva becomes stratified keratinized epithelium

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11
Q

What is an example of Mesenchymal Metaplasia?

A

Myositis Ossificans

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12
Q

What is Myositis Ossificans?

A

Muscle tissue changes to bone during healing

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13
Q

Is Dysplasia reversible?

A

Yes, if the driving stressor is removed

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14
Q

Is Carcinoma reversible?

A

No

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15
Q

What is this?

A

Left Ventricular Hypertrophy

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16
Q

What is this?

A

Barrett Esophagus

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17
Q

What is this?

A

Keratomalacia

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18
Q

What is this?

A

Myositis Ossificans

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19
Q

Which is more susceptible to ischemic injury, neurons or skeletal muscle?

A

Neurons

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20
Q

How long can a neuron last without oxygen before injury occurs?

A

3-5 Minutes

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21
Q

Define SaO2

A

Hemoglobin Oxygen Saturation

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22
Q

Define PaO2

A

Partial Pressure of 02 in the arteries

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23
Q

Put the following in the correct order (for inspiration).

PaO2

SaO2

FiO2

PAO2

A

FiO2 → PAO2 → PaO2 → SaO2

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24
Q

What 3 things can cause ischemia?

A
  1. Decreased arterial perfusion
  2. Decreased venous drainage
  3. Shock (generalized hypotension)
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25
Q

What is the difference between Ischemia and Hypoxemia?

A

Ischemia is decreased blood flow through an organ and Hypoxemia is low partial pressure of O2 in the blood

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26
Q

What is Budd-Chiari syndrome?

A

Thrombosis of hepatic vein which can lead to liver infarction.

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27
Q

What 2 things can cause Budd-Chiari syndrome?

A
  1. Lupis hypercoagulability
  2. Polycythemia Vera
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28
Q

What happens to PaO2 and SaO2 in anemia?

A

Both remain at nomral values.

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29
Q

What effect does CO poisoning have on PaO2 and SaO2?

A

PaO2 is normal

SaO2 decreases

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30
Q

What 3 things can cause CO poisoning?

A
  1. Smoke from fires
  2. exhaust from cars

3. gas heaters

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31
Q

What is Methemoglobinemia?

A

Iron in heme is oxidized to Fe3+ which can’t bind O2

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32
Q

What causes Mehemoglobinemia?

A

Oxidant stress (sulfa and nitrate drugs)

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33
Q

What is the classic finding of Mehemoglobinemia?

A

Cyanosis with chocolate colored blood

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34
Q

What is the treatment for Methemoglobinemia?

A

Intavenous Methylene Blue

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35
Q

ATP is low during hypoxia. What 3 things does this affect?

A
  1. Na+-K+ pump
  2. Ca2+ pump
  3. aerobic glycolysis (increase in lactic acid)
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36
Q

What is the hallmark of reversible injury?

A

Cellular Swelling

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37
Q

What 3 things are characteristic of cellular swelling?

A
  1. loss of microvilli
  2. membrane blebbing
  3. swelling of the RER and dissociation of ribosomes (decreased protein synthesis)
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38
Q

What is the hallmark of irreversible injury?

A

Membrane Damage

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39
Q

What 3 cellular membranes are damaged by hypoxia?

A
  1. Plasma Membrane
  2. Mitochondrial Membrane
  3. Lysosome Membrane
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40
Q

What is the hallmark of cell death?

A

Loss of the Nucleus

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41
Q

What are the 3 steps in the loss of the nucleus in cell death?

A
  1. pyknosis (nuclear condensation)
  2. karyohhexis (fragmentation)
  3. Karyolysis (dissolution)
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42
Q

What are the two mechanisms of cell death?

A
  1. Necrosis
  2. Apoptosis
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43
Q

Which are Necrosis and which are Apoptosis?

  1. Large vs Small group of cells that die
  2. Physiologic vs Pathologic
  3. Followed by inflammation or not
A

Necrosis

  1. Large group of cells
  2. never physiologic
  3. followed by acute inflammation

Apoptosis

  1. Small Group of cells
  2. Physiologic
  3. NOT followed by inflammation
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44
Q

Which pattern of necrosis has

necrotic tissue that remains firm due to coagulation of proteins, but no nucleus?

A

Coagulative

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45
Q

Which pattern of necrosis is

characteristic of Brain infarction, Abcesses, and Pancreatitis?

A

Liquefactive

46
Q

In liquefactive necrosis of the brain, what liquefies the brain?

A

Microglial

47
Q

In liqufactive necrsis in an abcess, what liqufies the tissues?

A

Neutrophils

48
Q

In liquefactive necrosis of the Pancreas, what liquefies the Pancrease?

A

Preoteolytic enzymes from the pancreas

49
Q

Which pattern of necrosis has

A chalky-white appearance?

A

Fat Necrosis

50
Q

Which pattern of necrosis is

associated with mialignant hypertension and vasculitis?

A

Fibrinoid

51
Q

Which pattern of necrosis is characterized by

soft and friable necrotic tissue with a “cottage cheese-like” appearance?

A

Caseous Necrosis

52
Q

Which pattern of Necrosis is

Caused by TB or fungal infection

A

Caseous Necrosis

(granulomatous inflammation)

53
Q

Which pattern of necrosis is

known to resemble mummified tissue?

A

Gangrenous Necrosis

54
Q

Which pattern of necrosis is

a mixture between coagulative and liqufactive necrosis?

A

Caseous Necrosis

55
Q

Which pattern of necrosis is

characteristic of ischemia of the lower limb and GI

A

Gangrenous Necrosis

56
Q

What happens when gangrenous tissue becomes infected?

A

Wet Gangrene (liquefactive necrosis)

57
Q

Which pattern of necrosis is

characteristic of ischemic infaction to all organs except for the brain?

A

Coagulative Necrosis

58
Q

Which pattern of Necrosis is

found in trauma to the breast?

A

Fat Necrosis

59
Q

Saponificatoin is a part of which pattern of Necrosis?

A

Fat Necrosis

60
Q

What is the difference between dystrophic and metastatic calcificatoin?

A

Dystrophic is caused by Calcium deposition on dead tissues

Metastatic involves high serum Ca or K and Ca deposition on living tissues.

61
Q

Is saponification metastatic or dystrophic calcification?

A

Dystrophic

62
Q

Which pattern of necrosis is

characterized by damage to blood vessel walls by leaking proteins?

A

Fibrinoid Necrosis

63
Q

C is normal kidney tissue.

What does B demonstrate?

A

Coagulative Necrosis

64
Q

What is this an example of?

A

Dry Gangrenous Necrosis

65
Q

What is this an example of?

A

Caseous Necrosis

66
Q

What is this an example of?

A

Fat Necrosis

67
Q

What is this an example of?

A

Fibrinoid Necrosis

68
Q

What is this an examle of?

A

Apoptosis

69
Q

What are some examples of Apoptosis?

A
  1. Endometiral shedding
  2. Removal of cells during embryogenesis
  3. CD 8+ T cell-mediated killing of virally infected cells
70
Q

Apoptosis is mainly mediated by what?

A

Caspases

71
Q

What do caspases do?

A

activate proteases and endonucleases

72
Q

what are the 3 steps of apoptosis?

A
  1. chell shirnks
  2. nucleus condenses and fragments
  3. apoptotic bodies fall from cell and are removed by macrophages
73
Q

What are the 3 Caspase activation pathways and what are their mechanisms?

A
  1. Intrinsic Mitochondrial pathway

(cytrochrome C activates Caspases)

  1. Extrinsic receptor ligand pathway

(FAS ligand & FAS death receptor/TNF & TNF receptor)

  1. Cytotoxic CD8+ T-Cell mediated pathway

(perforins create pores, granzymes enter and activate caspases)

74
Q

The extrinsic receptor-ligand pathway of caspase activatoin foudn in the body?

(FAS death receptor and FAS ligand)

A

Negative selection of thymocytes in the thymus

75
Q

How are free radicals formed physiologically?

A

Partial reduction of O2 in oxidative phosphorylation

76
Q

What are the 4 potential products of the reduction of O2 (and how many electrons does it accept to form them)?

A

1 e- O2-

2 e- H2O2

3 e- -OH

4 e- H2O

77
Q

Which of the physiological free radicals is the most dangerous?

A

Hydroxy radicals

78
Q

Which enzyme deals with each of the O2 derived free radicals?

A

O2- Superoxide Dismutase (SOD)

H2O2 Catalase

-OH Glutathione peroxidae

79
Q

What are the 3 mechanisms for eliminating free radicals?

A
  1. Antioxidants (Vit A,C,E)
  2. Enzymes
  3. Metal Carrier Proteins (transferrin & ceruloplasmin)
80
Q

What are the 4 pathological methods of generating free radicals?

A
  1. Ionizing Radiation (-OH)
  2. Inflammation (NADPH Oxidase uses them to kill)
  3. Metals (Fe and Cu)
  4. Drugs and Chemicals (P450 system)
81
Q

What disease is characterized by the excess of Fe?

(and what reaction is the mechanism for the damage?)

A

Hemochromatosis

(Fenton Reactoin makes -OH)

82
Q

What disease is characterized by an excess of serum Cu?

(and what is ti that causes the damage?)

A

Wilson’s disease

(free radicals)

83
Q

What chemical is commonly associated with the Dry Cleaning Industry?

A

CCl4

(Carbon TetraChloride)

84
Q

What is the mechanism of damage of CCl4?

(and what does it lead to?)

A
  1. P450 system converts it to the free radical CCl3
  2. Causes cell injury and swelling of RER which inhibits protein synthesis
  3. decreased apolipoproteins lead to fatty change in the liver.
85
Q

What is reperfusion injury?

A

returning blood to ischemic tissue causes generation of O2 derived free radicals.

86
Q

If a patient experiences a rise in cardiac enzymes then they probably have cardiac ischemia. What do they have if the enzymes condinue to rise after treatment?

A

Reperfusion Injury

87
Q

What is an amyloid and where is it (histologically)?

A

A misfolded protein that deposits in the extracellular space.

88
Q

What are the 2 mian characteristics of an amyloid protein?

A
  1. β-pleated sheet
  2. Congo red stain

(apple-green birefringence under polarized light)

89
Q

Primary amyloidosis is systemic deposition of which type of amyloid?

A

AL Amyloid

90
Q

Primary amyloidosis is associated whith what type of disease?

A

Plasma Cell Dyscrasias (Multiple Myeloma)

91
Q

AL amyloid is derived from what?

A

Immunoglobulin Light Chain

92
Q

Secondary Amyloidosis is the systemic deposition of what?

A

AA Amyloid

93
Q

From what is AA Amyloid derived?

A

Serum Amyloid-Associated protein (SAA)

94
Q

SAA is found in what conditions?

A
  1. Chronic Inflammation
  2. Malignancy

3. Familial Mediterrainian Fever (FMF)

95
Q

FMF is due to a dysfunction of what?

A

Neutrophils

96
Q

What mode of inheritance is associated with FMF?

A

Autosomal Recessive

97
Q

Which organ is most commonly involved in systemic amyloidosis?

A

The Kidney (Nephrotic Syndrome)

98
Q

How is amyloidosis diagnosed?

A

Biopsy

(often from abdominal fat pad and rectum)

99
Q

How are organs damaged by amyloidosis treated?

A

Amyloidosis cannot be removed and the organs must be transplanted.

100
Q

What are the 6 types of local amyloidosis?

A
  1. Senile Cardiac Amyloidosis
  2. Familial Amyloid Cardiomyopathy
  3. Non-Insulin-Dependent Diabetes Mellitus
  4. Alzheimer Disease
  5. Dialysis Associated Amyloidosis
  6. Medullary Carcinoma of the Thyroid
101
Q

What is the protein associated with Senile Cardiac Amyloidosis?

A

Non-mutated Serum Transthyretin

102
Q

What is the main symptom of Senile Cardiac Amyloidosis?

A

Asymptomatic

103
Q

What is the protein associated with Fmailiial Amyloid Cardiomyopathy?

A

Mutated Serum Transthyretin

104
Q

What condition does Familial Amyloid Cadriomyopathy lead to?

A

Restrictive Cardiomyopathy

105
Q

What is the protein associated with Amyloids of Non-Insulin-Dependent Diabetes Mellitus?

A

Amylin (derived from Insulin)

106
Q

What is the amyloid associated with Alzheimer’s Disease?

A

Aβ amyloid

(derived from β-amyloid precursor protein aka β-APP)

107
Q

On which chromosome is the gene for β-APP located?

What is the significance of this?

A

Chromosome 21

People with Down Syndrome develop Alzheimer disease earlier.

108
Q

What protein is the amyloid in Dialysis-associated Amyloidosis?

Where does it deposit?

A

β2-microglobulin (a component of MHC-I)

It deposits in the joints

109
Q

What is the mechanism of amyloidosis in a patient with Medullary carcinoma of the thyroid?

A

Calcitonin is over-produced by tumor cells and deposits in the tumor.

110
Q

How is the thyroid biopsied?

A

fine needle aspiration

111
Q

What is described as tumor cells in an amyloid background?

A

Amyloidosis in Medullary carcinoma of the thryoid

Pathoma (4 decks)

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