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Alya Cards Pathology Robbins basis > Ch 2 > Flashcards

Ch 2 Flashcards

1
Q

Causes of cell injury (7)

A

1.Oxygen deprivation
2.physical agents
3. Chemical/drugs
4.genetic
5.nutritional imbalances
6.infectious agents
7.immunologic

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2
Q

Give an example of hypoxia causing cell injury?

A

Acute Occlusion of blood vessels - ischemia leading to cell injury

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3
Q

Give an example of physical agents causing cell injury?

A

Trauma (mechanical), temperature (burns), sudden atmospheric pressure changes, electives shock

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4
Q

Give an example of immunologic agents that cause cell injury?

A

Viruses
Tapeworms
Parasites
Fungi

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5
Q

What time frame would ischemic changes be seen in light microscopy?

A

4-12 hrs after onset of ischemia

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6
Q

Is swelling of cell reversible?

A

Yes if happens in minutes

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7
Q

When does cell swelling become irreversible? (Timeframe)

A

1-2 hrs

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8
Q

In what order can you see changes in cells (chemical—>macro)

A

Minutes to hours:
1.biochemical
2.Ultrastructural

Hours to days:
3.Light micro
4.gross morphologic changes

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9
Q

What are features of necrosis:
1.cell size (swelling)
2.nucleus
3.plasma membrane
4.cellular contents
5.adjacent inflammation
6.physiologic/pathologic?

A

1.enlarged
2.karyorrhexis/pyknosis/karyolysis
3.disrupted
4.enzymatic digestion/leak out of cell
5.frequent
6.pathologic

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10
Q

What are features of apoptosis:

1.cell size (swelling)
2.nucleus
3.plasma membrane
4.cellular contents
5.adjacent inflammation
6.physiologic/pathologic?

A

1.reduced/shrink
2.fragmentation into nucleosome-size fragments
3.intact however altered structure
4.intact-may be released into apoptotic bodies
5.none
6.physiologic mainly, can be pathologic after cell injury (eg DNA damage)

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11
Q

Why do cells swell when injured?

A

Influx of water due to failure of ATP dependent Na-K channel (due to failure of mitochondrial oxyfative phosphorylation)

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12
Q

What effect does cell death have on tissues? (Colour, weight, turgor)

A

Pale
Heavier
Increased turgor

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13
Q

What are the early changes in cells in injury? (Reversible and irreversible)

A

1.swelling of cell and organelles
2.blebbing of plasma membrane
3.detachement of ribosomes from ER
4. Chromatin clumping

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14
Q

What are vacuoles?

A

Pinched off segments of ER

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15
Q

What colour does eosinophils take when dyed with H&E dye during cell death?

A

Red

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16
Q

Why no blue dye seen with H&E during cell death?

A

RNA binds haematoxylin blue - RNA is lost in cell death

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17
Q

What are ‘myelin figures’?

A

Phospholipid aggregates from destroyed lipid membranes - seen in cell injury

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18
Q

What are the ultrastructural changes that can be seen in cell injury (5)

A

1.plasma membrane alterations eg blebbing, blunting, loss of microvilli
2.mitochondrial changes: swelling and appearance of small densities
3.myelin figures
4.Dilatation of ER
5.nuclear alterations

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19
Q

What are the characteristics of necrosis (4)

A

1.denaturation proteins
2.leakage contents through damaged cell membrane
3.enzymatic digestion
4.local inflammation

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20
Q

Necrosis: what are the possible patterns of nuclear change? 3

A
  1. Karyolysis: basophilia within chromatin fading
  2. Pyknosis: nuclear shrinkage, increased basophilia
    3.karyorrhexis: pyknotic nuclear fragmentation (happens after pyknosis)
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21
Q

What are the characteristics of irreversible injury? 2

A
  1. Mitochondrial dysfunction
  2. Cell membrane dysfunction
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22
Q

What are the characteristics of mitochondrial dysfunction in irreversible cell injury?

A

1.Loss of oxidative phosphorylation
2. Loss of ATP generation

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23
Q

Example of Liquefactive necrosis?

A

Bacterial/fungal infection into tissues

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24
Q

What is Liquefactive Necrosis?

A

Cell death and gets digested to form a liquid (accumulation of leukocytes)

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25
Q

What is coagulative necrosis?

A

1.Secondary Occlusion of blood supply
2. Cell death with preserved architecture

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26
Q

What are the characteristics of coagulative necrosis?

A
  1. Preserved architecture
    2.high eosinophils (red nuclei)
    3.firm texture
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27
Q

What is an infarct?

A

Localised area of coagulative necrosis

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28
Q

What are the macro characteristics of Casseous necrosis?

A

1.cheeselike appearance (white, friable)
2. Structure less
3.granular debris within inflammatory border

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29
Q

Wet gangrene is (type of necrosis)

A

Liquefactive necrosis

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30
Q

Infarct to brain is (type of necrosis)

A

Liquefactive (unknown reason)

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31
Q

What is fat necrosis?

A

Focal areas of fat destruction (eg pancreatitis, leakage of lipases from acinar cells into abdominal cavity)

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32
Q

Macroscopic appearance of fat necrosis?

A

Chalky white appearance (fatty acids + calcium deposits) eg fat saponification

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33
Q

What is fibrinoid necrosis?

A

Vascular damage: immune reaction within blood vessels (antigen/antibody vs vessel wall)

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34
Q

What is the appearance of fibrinoid necrosis in H&E stains?

A

Bright pink (protein complexes/antibodies leak out from cells)

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35
Q

What are apoptotic bodies?

A

Plasma-membrane walled nuclear fragments (has fragments of nucleus and cytoplasm)

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36
Q

What are the 2 pathways for apoptosis?

A
  1. Intrinsic (mitochondrial) pathway
    2.Extrinsic (death receptor) pathway
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37
Q

Apoptosis: _______ initiates enzymatic segregation of proteins and DNA in a cell

A

Caspases

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38
Q

What are the triggers of apoptosis?

A
  1. DNA damage
    2.loss of survival signals
  2. Misfolded proteins (ER stress)
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39
Q

What is the role of BCL2 family in apoptosis?

A

Inhibits apoptosis

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40
Q

Viral infections eg HIV are a type of (cell death)

A

Apoptosis

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41
Q

What is the morphology of cells undergoing apoptosis?

A
  1. Cell shrinkage
    2.chromatin condensation (characteristic)
  2. Formation of cytoplasmic blebs/apoptotic bodies
    4.phagocytosis of apoptotic cells (by macrophages)
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42
Q

Apoptosis: What protein is released in the mitochondrial pathway?

A

Cytochrome C

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43
Q

Apoptosis: the release of cytochrome C is dependent on —– integrity

A

Mitochondrial wall

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44
Q

How does BCL2 do it’s anti apoptotic function?

A

Located outside mitochondrial membrane: makes membrane impermeable to prevent leakage of cytochrome c

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45
Q

Apoptosis: what are the pro-apoptotic signals in the mitochondrial pathway?

A

BAX/BAK

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46
Q

Intrinsic mitochondrial pathway: what is the role of BAD/BIM/Puma/Noxa?

A

Regulated pro apoptotic initiators: have the ability to activate BAX/BAK to increase mitochondrial permeability

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47
Q

How does cytochrome C cause apoptosis?

A

Binds to APAF1 –>forms an apoptosome–>bind to caspase9–>activate more caspases

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48
Q

Apoptosis: IAP inhibition causes____

A

Initiation of caspase cascade

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49
Q

Apoptosis: IAP stands for ____

A

Inhibitors of Apoptosis

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50
Q

What is the role of IAP in apoptosis?

A

To prevent inappropriate activation of caspase

51
Q

Death receptors are members of ____ family

A

TNF

52
Q

Example of death receptors?

A

Type 1 TNFR
Fas (CD95)

53
Q

The extrinsic (death receptor) pathway activates which caspases?

A

Caspase 8 and 10

54
Q

What is efferocytosis?

A

Phagocytosis of apoptotic cells

55
Q

Necroapoptosis is triggered by ligation of ____ and ____ viruses

A

TNFR1
DNA/RNA viruses

56
Q

Necroapoptosis depends on _____ complex.

A

RIPK1/RIPK3

57
Q

Necroapoptosis: RIPK signalling leads to _____ (process) which then forms _____in plasma membrane

A

Phosphorylation on MLKL
Pores

58
Q

Pyroapoptosis: involves activation of _____ which then cleaves ____into active form.

A

Caspase1
IL1

59
Q

What is Ferroapoptosis?

A

Excessive iron or ROS overwhelm glutathione dependent antioxidant defenses—>lipid peroxidation

60
Q

Formation of mammalian growth plate is an example of (cell death)

A

Necroapoptosis

61
Q

Examples of necroapoptosis?

A

1.mammalian growth plate
2.acute pancreatitis
3.ischemia-reperfusion injury
4. Parkinson’s disease
5.CML infections

62
Q

What is autophagy?

A

Cell eats own contents

63
Q

Steps of autophagy?

A

1.nucleation and formation of isolation membrane (phagophore)
2. Formation of a vesicle (autophagosome)
3.maturation and fusion with lysosomes

64
Q

____ (marker) is increased during autophagy.

A

PE-lipidated LC3

65
Q

Examples of autophagy?

A
  1. Alzheimer’s
    2.Crohns
    3.HSV-1
    4.some cancers
66
Q

Diseases caused by misfolding proteins?

A

1.Alzheimers (AB protein)
2. Cystic fibrosis (CFTR - transmembrane regulator)
3.Alpha1 antitripsyn deficiency

67
Q

High intracellular (Ion) causes cell injury

A

Calcium

68
Q

Endonucleases (role)

A

Fragment DNA and chromatin

69
Q

Phospholipase (role)

A

Damage cell plasma membrane

70
Q

Intracellular Ca is sequestered in ____ and ____

A

ER and mitochondria

71
Q

DNA damage activates apoptosis by ____ pathway

A

P53 dependent

72
Q

Why does ischemia cause faster cell damage than hypoxia?

A

1.unable to supply substrates through blood for anaerobic glycolysis
2. Unable to clear out metabolites, stops glycolysis

73
Q

What transcription factor is released in hypoxia induced stress?

A

HIF-1 (Hypoxia Inducible Factor)

74
Q

What are the 3 ways ischemia causes cell death?

A

Reduction in ATP leads to:
1. Failure of Na+ pump>influx of Ca+, H2O, Na+, Efflux K+>ER, cell swelling
2.increased anaerobic glycolysis>decreased glycogen, PH and increased lactic acid>clumping chromatin
3.detachment ribosomes>decreased protein synthesis

75
Q

Ischemia-reperfusion: What is the mechanism of which oxidative stress causes injury?

A

1.Damaged cells>Incomplete reduction in O2 in leukocytes >free radicals and Nitrogen
2.complement system: IgM deposits during ischemia, complement binds when reperfusion happens
3.influx calcium from blood

76
Q

How do chemicals/toxins cause cell injury? 2

A
  1. Direct: mercury poisoning vs liver
    2.indirect: formation of toxic metabolites: eg cytochrome P450 conversion of CCL4 to CCL3 (dry cleaning)
77
Q

Example of physiologic hypertrophy?

A

Estrogen enlarging uterus during pregnancy

78
Q

What are the triggers that activate transcription factors in cardiac hypertrophy? 3

A
  1. Mechanical stretch
  2. Agonists (eg angiotensin, Alpha adrenergic hormones)
  3. Growth factors (IGF-1)
79
Q

Cardiac hypertrophy: what are the transcription factors? 3

A

GATA4, NFAT, MEF2

80
Q

Cardiac hypertrophy: How do transcription factors increase hypertrophy?

A
  1. Synthesis of contractile proteins
    2.induction of fetal genes eg ANF, cardiac alpha actin (decrease workload, increase contractility)
    3.prosuce more growth factors
81
Q

Atrophy: what pathway leads to protein degradation?

A

Ubiquitin-proteasome pathway

82
Q

What can cause atrophy?

A

1.disuse
2.inadequate nutrition
3.pressure eg mass compressing
4.ischemia
5.loss of endocrine stimulation
6.loss of innervation
7.decreased workload

83
Q

What is a common example of metaplasia in epithelium?

A

Columnar to squamous eg respiratory tract (bronchi, trachea) in smoker

84
Q

Barrets oesophagus converts ____ to ____ epithelium.

A

Squamous to columnar

85
Q

Myositis ossificans is a type of ____

A

Metaplasia (bone formation in muscle)

86
Q

Atrophy is associated with increased (cell death type)

A

Autophagy

87
Q

What is a Xanthoma?

A

Intracellular accumulation of cholesterol within macrophages

88
Q

What enzyme is defective in Werner syndrome?

A

DNA Helicase (unable to repair DNA>cell aging prematurely)

89
Q

What are the mechanisms involved in cell aging?

A

1.DNA damage
2.Cell senescence (stop dividing): telemere shortening
3.defective protein homeostasis

90
Q

Telomere shortening is involved in which diseases? 2

A
  1. Aplastic anaemia
    2.pulmonary fibrosis
91
Q

What molecular structure maintains correct folding of proteins?

A

Chaperones

92
Q

What is the mechanism of which caloric restriction increases longevity? 2

A
  1. ILGF-1
  2. Sirtuins
93
Q

Lipofuscin

A
94
Q
A

Lipofuscin granules within cardiac myocytes

95
Q

How is melanin formed?

A

Tyrosine > dihydroxyphenylalanine

Catalysed by tyrosinase

96
Q

What are psamomma bodies? Where are they seen?

A

Necrotic tissues with mineral deposits (seen in papillary cancer)

97
Q

What are the 4 causes of hypercalcaemia?

A
  1. Increased secretion of PTH
  2. Resorption of bone tissue
  3. Vitamin D disorders (vit D intoxication)
    4.renal failure
98
Q

What are examples of exogenous pigments?

A

Carbon

99
Q

What is an example of endogenous pigments?

A

1.melanin
2.lipofuscin
3.haemosiderin

100
Q

Lipofuscin is a breakdown product of ____

A

Lipid peroxidation

101
Q

Which part of renal tubules absorb protein?

A

Proximal tubule (via pinocytosis)

102
Q

What are Russell bodies?

A

Eosinophilic inclusions from Distended ER from accumulation of protein

103
Q

Keratin filaments are found (cell type)

A

Epithelial cells

104
Q

Neuro filaments are found in (cell)

A

Neurons

105
Q

Desmin filaments are found in (cell)

A

Muscle cells

106
Q

Vimentin filaments are found in (cell)

A

Connective tissue

107
Q

Glial filaments are found in (cell)

A

Astrocytes

108
Q

What are the steps of the inflammatory reaction? 5

A

1.recognition
2.recruitment
3.removal
4.regulation
5.repair

109
Q

Inflammatory Rx: what cells involved in Acute Respiratory Distress syndrome (ARDS)?

A

Neutrophils

110
Q

Which filament collects in damaged hepatocytes?

A

Intermediate filaments (Mallory Hyaline)

111
Q

What are the BH1-4 proteins?

A

Inhibitors of apoptosis
BCL-2, BCL-XL, MCL-1

112
Q

How do free radicals cause cell injury?

A

Destroy phospholipid in cell membrane

113
Q

What is the peptide that macrophages have that kill microbes?

A

Cathelicidin - vitamin D dependent

114
Q

What chemical mediates migration of leukocytes to site of injury?

A

Chemokines

115
Q

What substance activates macrophages and monocytes?

A

IFN Y

116
Q

How are abscesses formed?

A

Neutrophils release lysosomes

117
Q

Recurrent infections in chronic granulomatous disease is caused by

A

Defect in neutrophil oxygen dependent killing of bacteria

118
Q

What does C3b do?

A

Facilitates phagocytosis

119
Q

Which molecule is responsible for rolling of neutrophils on endothelium?

A

Selectins

120
Q

What is the role of C5a in immunity?

A

Chemotactic: neutrophil activation

121
Q

Which chemokines (2) can increase vascular permeability by histamine release from mast cells?

A

C3a and C5a

122
Q

Serous vs fibrinous inflammation

A

Both involve mesothelial surfaces eg pericardium

Serous : protein poor fluid
Fibrinous: protein rich (precipitation of fibrin)

123
Q
A

Psamomma body

124
Q
A

Russell body

Alya Cards Pathology Robbins basis (12 decks)

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