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Robbins Pathology MOD1 (Chptr 1-6) > Chapter 2 > Flashcards

Chapter 2 Flashcards

1
Q

IN the intrinsic pathway, what neutralization of which factor allows for apoptosis

A

IAPs

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2
Q

Which tissue almost always undergoes liquefactive necrosis

A

CNS during hypoxic events

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3
Q

Which pathway is the major pathway of all mammalian cells

A

Intrinsic mitochondrial pathway

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4
Q

What are the conditions that commonly cause metaplstic calcification

A

1) Increased PTH
2) Resorption of bone tissue
3) Vitamin D related disorders
4) Renal failure

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5
Q

How does increased calcium levels in the cause death

A

Opening of transition pore, activates phospholipase (breaks membranes), proteases, endonucleases (DNA damage) and ATPases, and caspases

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6
Q

How do Striated and cardiac muscle respond to increased metabolic demands

A

Hypertrophy

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7
Q

FASL is expressed on which cells

A

T cells that recognize self antigens

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8
Q

What is lipofuscin and what is it derived from

A

Aka lipochrome, which is an insoluble pigment and is derived through lipid peroxidation of polyunsaturated lipids

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9
Q

How does mercuric chloride poisoning cause damage

A

Mercer’s binds to sulfhydryl of cell membranes. Leads to increase in permeability

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10
Q

What are four conditions associated with autophagy defects

A

1) Cancer
2) Neurodegenerative disorders
3) Infectious diseases
4) IBD

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11
Q

What is marasmus

A

Prolonged protein-calorie malnutrition leading to muscle wasting for energy

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12
Q

What is the result of the defective protein in familial hypercholesterolemia

A

Hypercholesterolemia

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13
Q

What are the 2 proapoptotic proteins

A

BAK and BAX

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14
Q

What is the condition of metastatic calcification

A

Deposition of calcium salts in healthy tissue

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15
Q

How does muscle accomplish hypertrophy

A

Increase in protein synthesis, along with increase in number of myofilaments. This increases the contraction strength of muscle

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16
Q

What is the fate of cells that are hormone sensitive and do not receive their relevant hormone

A

Undergo apoptosis via intrinsic pathway (lack of BCL2/BCL-XL and increase in BIM)

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17
Q

How do the myosin heavy chain isotypes different in hypertrophy muscles

A

In muscle hypertrophy, alpha is replaced with beta (slower and more efficient contraction)

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18
Q

What is the process of activation for the FAS death receptors

A

1) FASL binds to the FAS receptor
2) FADD is grouped together and activated caspase 8
3) Caspase 8 activated the executioner proteins

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19
Q

What is the defective protein in Alpha 1 antitrypsin deficiency

A

Alpha 1 antitrypsin

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20
Q

What is the protein disorder in familial hypercholesterolemia

A

LDL receptor

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21
Q

What is the effect of rapamycin

A

Blocks the mTOR pathway, which increases longevity of life due to decreased cell cycle progression.

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22
Q

What is dystrophic calcification

A

Deposition of calcium salts and other minerals into necrotic tissue and debris that is not destroyed

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23
Q

What is the defective protein in tay-Sachs

A

Hexosaminidase Beta subunit

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24
Q

What level of ATP depletion will result in widespread effects

A

5-10%

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25
Q

What is karyorrhexis

A

Nucleus will undergo fragmentation

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26
Q

What is the affect of vitamin A deficiency in the respiratory epithelium

A

Induces squamous metaplasia

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27
Q

In Alzheimer disease, what is the relation to autophagy

A

Accelerated autophagy, with any defects in autophagy accelerating the disease

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28
Q

Death receptor is part of which family of receptors

A

TNF family

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29
Q

What is the mechanism of deactivation for hydroxyl ion

A

Conversion to water by glutathione peroxidase

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30
Q

What are cholesterolosis

A

Accumulation of cholesterol filled macrophages in the gallbladder

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31
Q

What are the characteristics of caseous necrosis

A

Often with a tuberculous infection, where there is the formation of a granulosa

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32
Q

How does necroptosis differ from apoptosis

A

Caspase independent

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33
Q

What is pyknosis

A

Irreversible condensation of chromatin (nuclear shrinkage) and basophils

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34
Q

What is the ion in cytosolic SOD

A

Copper/Zinc

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35
Q

What is the mitochondrial permeability tradition pore and what triggers it

A

High conductance channel that allow loss of mito membrane potential that leads to depletion of ATP and necrosis of cell. Triggered by mito damage

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36
Q

How doe cyclosporine affect the mitochondrial permeability transition pore

A

Prevents the pore from forming via blocking the key protein cyclophilin D, which will help prevent mito necrosis and death

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37
Q

What leads to coagulative necrosis in all tissues except one

A

Obstruction of a vessel will lead to coagulative necrosis in all tissue except the brain

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38
Q

Which type of cells express levels of telomerase

A

Germ cells have high expression, which stem cells have some lower expression

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39
Q

What is direct chemical toxicity

A

Chemical directly causes the damage to the cell by binding to crucial components

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40
Q

What is the result of the defective protein in Tay-Sachs

A

Lack of lysosomal enzyme that eats to storage of the GM2 gangliosides in neurons

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41
Q

What are residual bodies

A

Cellular debris that resists degredation and persists in autophagic vacuoles

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42
Q

What does the gene CDKN2A code for

A

A tumor suppressor gene contains p16 or INK4a, which can halt the cell cycle progression

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43
Q

How does calorie restriction lead to longevity of life via IGF1

A

IGF1 triggers glucose availability and the progression to cell division and anabolism. So decreasing IGF1 will decrease the progression through cell cycles

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44
Q

Hyperplasia is a common response to which pathogens

A

Viral infections, such as papillomaviruses, which cause hyperplastic epithelium (interference of host regulatory proteins)

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45
Q

What is the most common cause of fatty liver in developed countries

A

Alcohol abuse and nonalcoholic fatty liver associated with obesity and diabetes

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46
Q

What are the domains on the antiapoptotic proteins

A

Contains 4 BH regions

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47
Q

What is the process of cytochrome C binding

A

1) APAF1 (apoptosis activating factor 1)
2) Caspase 9 (initiator)
3) SMAC/Diablo activation
4) #3 binds to IAPs(which are inhibators of apoptosis)
5) Activation of Caspase 3 (executioner)

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48
Q

What are the two pathways involved in hypertrophy

A

1) PI3K/AKT pathway (exercise induced hypertrophy)

2) GCPRs Pathway ( pathological hypertrophy)

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49
Q

What is the mechanism of deactivation for hydrogen peroxide

A

To water and oxygen by catalase (peroxisomes) or glutathione perioxidase (cyto or mito)

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50
Q

What are the enzymes and complexes activated by necroptosis

A

1) TNFR1 is activated
2) Receptor associated kinase 1 and 3 (RIP 1 & 3)
3) RIP1/3 complex recruits caspase 8
4) Caspase 8 activation —> apoptosis
5) Caspase 8 not Activated —> necroptosis

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51
Q

How does hypoxia lead to depletion of glycogen stores

A

1) No oxygen leads to decreased ox phos
2) Decreased ATP and Increased AMP —> stimulation of PKF (increased glycolysis) and phosphorylase activity (increased glycogen breakdown)
3) Increased substrate level phosphorylation

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52
Q

What are Xanthomas what are they associated with

A

Intracellular accumulation of cholesterol within macrophages in the connective tissue of skin and tendons and associated with hereditary hyperlipidemia states

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53
Q

What is the function of hemosiderin

A

Golden yellow pigment that is the main storage of iron

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54
Q

What characteristics are associated with irreversible injury

A

Severe mitochondrial damage/ATP depletion, and rupture of lysosomes and plasma membranes,

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55
Q

What is the result of the misfolded protein in CJD

A

abnormal folding of PrPsc leads to neuron cell death

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56
Q

What type of protease is a caspase and what does it cleave

A

Cysteine protease and cleaves after aspartic residues

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57
Q

What is the common factor in tissue that are prone to metastatic calcification

A

All secrete acid and have an internal alkaline compartment

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58
Q

Once inhaled, what happens to the coal dust

A

Picked up by macrophages, taken through the lymph into the tracheobroncial lymph nodes. Accumulations of this leading to anthracosis (black lungs)

59
Q

What are the 3 ROS and their formula

A 
Superoxide anion (O2.  One electron)
Hydrogen peroxide (H2O2, two electrons)
Hydroxyl ion (.OH three electrons
60
Q

Macrophage deletion of autophagy gene Atg5 leads to susceptibility of which class of pathogens

A

Tuberculosis

61
Q

What are psammoma bodies and where are the commonly developed

A

Acquisition of calcification that look like grains of sand. Papillary cancers commonly develop psammoma bodies

62
Q

What are the main causes of hemosiderosis

A

1) increased dietary iron due to hemochromatosis
2) hemolytic anemia (increased lyses cells and free iron)
3) repeated blood transfusion

63
Q

What are the genes that are required for the creation of autophagosomes

A

Atgs

64
Q

What are the traits in cell injury that are reversible

A

Reduction in ox phos, depletion of ATP, cellular swelling , membrane Blebbing, detachment of the ribosomes from ER, and clumping of nuclear chromatin, loss of microvilli, amorphous densities, pinched off ER segments. (Hydropic change or vacuolar degeneration)

65
Q

What are the three antiapoptotic proteins

A

BCL2, BCL-XL, and MCL1

66
Q

What is the function of glutathione peroxidase

A

Protects against radical damage

67
Q

What are the characteristics of coagulative necrosis

A

A from texture, due to enzymes being denatured and therefore blocking degradation of dead cells. Associated with eosinophilia, anucleated cells

68
Q

What is the function of SOD

A

Superoxide anion to hydrogen peroxide

69
Q

How does the executioner capable differ in the intrinsic pathway versus the extrinsic pathway

A

Intrinsic uses caspase 9

Extrinsic uses 8 and 10

70
Q

What is the mechanism of inactivation of superoxide ion

A

To hydrogen peroxide and oxygen by SOD

71
Q

What is the ion in mitochondrial SOD

A

Manganese

72
Q

How many electrons are used and how much water is created for ETC

A

2H2, 4 electrons, O2 -> 2H2O

73
Q

What two reversible injury characteristics are visible under alight miscroscope

A

Cellular welling and fatty change (lipid vacuoles in cytoplasm) in Cells dependent on fat metabolism

74
Q

What is the enzymes seen in blood following hepatocyte damage

A

Transaminases

75
Q

What are the two things that bind to apoptotic bodies and help remove them

A

Thrombospondin (glycoprotein)

C1q

76
Q

What type of proteases are granzymes and where do they cleave

A

Serine proteases that cleave after aspartate residues

77
Q

What is the result of the defective protein in alpha 1 antitrypsin deficiency

A

Storage of non functional protein in hepatocytes that causes apoptosis and destruction of the elastic tissue leading to emphysema

78
Q

What are the triggers for hypertrophy

A 
Mechanical stress (major player in physiological, not pathological)
Vasoactive agents (Alpha adrenergic hormones,Angiotensin,endothelin-1)
Growth factors (TGF-Beta, IGF1, FGF)
79
Q

What is the most common exogenous pigment

A

Carbon (coal dust)

80
Q

Closure and elongation of the autophagolysosomes requires which protein, which can also be used to identify cells undergoing autophagy

A

LC3 (microtubule assocaited protein light chain 3

81
Q

What are the domains of the sensor proteins

A

One BH domain, aka BH3 only proteins

82
Q

What are the sensor proteins in apoptotic pathway

A

BAD, BIM, BID, Puma, Noxa

83
Q

What are the inducers and pathway of physiological hypertrophy

A

Mechanical stress and PI3K/AKT pathway

84
Q

What is the mechanism of deactivation for ONOO- (peroxynitrite anion)

A

Conversion to HNO2 by peroxiredoxins

85
Q

What is the only endogenous brown/black pigment

A

Melanin

86
Q

What would be the immediate histological changes in necrotic tissue

A

No changes from 4 to 12 hours, so we wouldn’t be able to see the damage

87
Q

The degredation of Cellular proteins during atrophy occurs via which pathway

A

Ubiquitin-proteasome pathway

88
Q

What are the characteristics of gangrenous necrosis

A

Applied to a limb that has lost blood supply and is undergoing apoptosis. (Wet-gagrene if bacteria is involved)

89
Q

What is the link between vitamin A and metaplasia

A

Vitamin A deficiency is associated with transcription factor dysregulation

90
Q

How does ischemia and hypoxia differ in timing and tissue damage

A

Hypoxia is just the lack of ox phos which ischemia is the loss of ox phos and all nutrients (no substrate phosphorylation). So damage is quicker and more severe during ischemia

91
Q

What is the role of TNF in cachexia

A

Seen in cancers and chronic inflammation. TNF suppresses appetite and lipid depletion, leading to muscle wasting

92
Q

What condition is associated with metastatic calcification

A

Hypercalcemia secondary to some disturbance in calcium metabolism

93
Q

Hypertrophy is defined as

A

Increase in size due to increase in production of cellular proteins

94
Q

What is the condition of dystrophin calcification

A

Deposition of calcium in dying tissue and occurs under normal calcium levels

95
Q

What are lipofuscins a sign of

A

Free radical injury and lipid peroxidation

96
Q

What are Russel bodies

A

ER distention and eosinophilia inclusions due to accumulation of proteins

97
Q

What are the conditions that can lead to increase resorption of bone

A

1) Primary tumors of bone marrow (multiple myeloma, leukemia)
2) Skeletal metastasis (breast cancer)
3) Accelerated bone turnover (Paget’s)
4) immobilization

98
Q

What is the enzymes seen in blood following cardiac damage

A

Troponin and creatine kinase

99
Q

What are the domains on the proapototic proteins

A

4 BH domains

100
Q

How does cyanide cause damage to the cell

A

Binds to mito cytochrome oxidase and inhibits ETC

101
Q

What is the function of catalase

A

Hydrogen peroxide to water

102
Q

What is Niemann-pick disease type C

A

Lysosomal storage defects in which the trafficking of the cholesterol leads to accumulations

103
Q

What is the role of FLIP and how can it be used

A

Binds to caspase 8 in the extrinsic pathway and blocks it. Can be used by pathogens to prevent the initiation of apoptosis

104
Q

What are the major causes of ATP depletion

A

Reduced oxygen supply, mito damage, toxins

105
Q

How to muscle atrophy differ with regards to acute decrease in workload compared to prolonged

A

Acute: decrease in size of fibers (reversible)
Prolonged: Decrease in number (apoptosis) (irreversible)and size, followed by bone resorption and osteoporosis

106
Q

What are the characteristics of liquefactive necrosis

A

Digestion of the necrotic tissue, and seen in focal bacterial and fungal infections. Creamy yellow pus.

107
Q

Why is myositis ossificans and what is it associated with

A

Bone formation in muscle, which can occur after intramuscular hemorrhage

108
Q

What is the most common stimulus for hypertrophy of muscle

A

Increased workload

109
Q

What is the enzymes seen in blood following liver damage (bile duct epithelium)

A

Alkaline phosphatase

110
Q

How is the Fenton reaction associated with ROS

A

Copper and iron require reduction for activation and can lead to ROS

111
Q

What is the result of increased anaerobic glycolysis

A

Increased lactic acid -> decreased pH -> breakdown of cellular enzymes —> clumping of nuclear chromatin

112
Q

What are the primary locations affected by metastatic calcification

A

Kidneys, lungs, gastric mucosa, pulmonary veins, and systemic arteries

113
Q

How is the complement system part of reperfusion injuries

A

IgM deposits in ischemic tissues, so when blood flow is reestablished, the complement proteins can now bind to the IgM

114
Q

What is the characteristic of the metaplasia in Barrett esophagus

A

Squamous cells to columnar cells (contain the goblet cells to help deal with the increased acid)

115
Q

What are Vitamin D related diseases that can cause metastatic calcification

A

1) vitamin D intoxification
2) sarcoidosis (macrophages activate Vit. D precursor)’
3) idiopathic hypercalcification of infancy (Williams syndrome)
4) abnormal sensitivity to vitamin D

116
Q

What is pyroptosis associated with

A

Fever caused by IL1

117
Q

What are the causes of repurfusion injury

A

Oxidative stress (reactive species), intracellular calcium levels, inflammation, complement system

118
Q

What is the most common genetic abnormality that leads to human cancers

A

Mutation in TP53

119
Q

In Huntington disease, what is the relation to autophagy

A

Mutant huntingtin impairs autophagy

120
Q

How does renal failure lead to hypercalcemia

A

Retention of phosphate, leading to secondary hyperPTHism

121
Q

How does ANP levels compare in hypertrophied cardiac muscle

A

ANP levels are higher in the cardiac hypertrophy (helps to upregulate the production of ANP to decrease the workload

122
Q

How is necroptosis similar to necrosis

A

-Permeable lysoszomes, ROS, damage to mito, reduction in ATP

123
Q

What is the defective protein in Alzheimer’s

A

Abeta peptide

124
Q

What are the end results seen in cell death via inflammasomes

A

1) Swelling of cell

2) Loss of membrane integrity and inflammatory response

125
Q

What are the caspases associated with inflammasomes and and pyroptosis

A

Caspase 1 and 11

126
Q

Increase in the number of autophagic vacuoles is an indication of what

A

Increased autophagy, commonly seen in atrophying muscles and cachexia

127
Q

Where are the enzymes that digest necrotic cells derived from

A

Lysosomes of dying cells themselves and lysosomes of recrutited inflammatory cells

128
Q

What is Werner syndrome

A

Inappropriate aging due to a defective DNA helicase

129
Q

What is the state of cellular senescence

A

Normal cells reach their limit of fixed number of cell divisions and become arrested in terminal non dividing state

130
Q

What are the transcription factors up-regulated to cause hypertrophy

A

GATA4, NFAT, MEF2

131
Q

What is causing alkaptonuria

A

Metabolic disease in which homogentisic (black pigment) is deposited in skin, connective tissue and cartilage, causing ochronosis

132
Q

What is the most common type of epithelial metaphasia

A

Columnar to squamous

133
Q

What is karyolysis

A

Chromatin will fade on H&E

Dissolution of nuclear due to RNA and DNAses

134
Q

How does CCL4 cause damage to the cell

A

1) CCL4 converted to .CCL3 by cytochrome P450 in ER of liver

2) Causes lipid peroxidation and damage

135
Q

What are the inducers and pathway of pathological hypertrophy

A

Vasoactive agonists/growth factors lead to the GCPR pathway

136
Q

How do necrotic cells stain on an H&E stain

A

Increased eosinophilia

137
Q

How does calorie restriction lead to longevity via Sirtuins

A

Sirtuins are an NAD dependent protein deacetylase. They are upregulated during high levels of NAD, and act as antioxidants, antiapoptotic and decrease metabolism

138
Q

What are the products and effects of excessive lipid breakdown

A

Products act as detergents and break up membranes

Unesterified free fatty acids, acyl carnitine, lysophospholipids

139
Q

What is the condition of hemosiderosis

A

Overload of iron that leads to deposition in organs and tissues

140
Q

What is hypoxia-inducible factor 1

A

Response to hypoxic environment that leads to new blood vessel formation, cell survival pathways, increased anaerobic glycolysis

141
Q

What is the relation of calcification and atherosclerosis

A

Calcification almost always present in atheromas of advanced atherosclerosis

142
Q

Most pathological hyperplasia is caused by

A

Excessive or inappropriate growth factors or hormones

143
Q

What is the condition of steatosis

A

Aka fatty change with abnormal accumulations of triglycerides in the parenchyma cells

144
Q

Proteinuria is assocaited with what changes in the kidney

A

Reabsorption droplets in the proximal renal tubule due to heavy protein leakage. Will diminish if proteinuria decreases

Robbins Pathology MOD1 (Chptr 1-6) (10 decks)

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