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Test 1 FTM > Lecture 7 > Flashcards

Lecture 7 Flashcards

1
Q

What is a neoplasm?

A

This is a new growth or an abnormal mass of cells

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2
Q

What are the two main groups of neoplasms?

A
  1. benign

2. Malignant

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3
Q

What are the behavioral and histological hallmarks of benign neoplasms?

A

Behavior:

  1. local growth only
  2. often in a capsule

Histology:

  1. resembles cell of origin
  2. few mitoses
  3. normal or slight increase in ratio of nucleus to cytoplasm
  4. cells are uniform throughout the tumor
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4
Q

What are the behavioral and histological hallmarks of malignant neoplasms?

A

Behavior:

  1. Invasive growth
  2. does not have a capsule around it

Histology:

  1. may show failure or cellular differentiation
  2. many mitoses, some are abnormal forms
  3. high nuclear to cytoplasmic ratio
  4. cells vary in shape and size
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5
Q

Define carcinoma?

A

This is a malignant tumor growing from epithelial tissue

many carcinomas affect glands that are involved with secretion

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6
Q

Define sarcoma?

A

A malignant tumor growing from connective tissues

Ex: cartilage, fat, muscle, tendons, and bones

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7
Q

leukemia?

A

Cancer of the blood or bone marrow

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8
Q

Melanoma?

A

malignant tumor of the melanocytes in the skin

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9
Q

Describe metastasis and how it occurs?

A

distant spread of tumor cells into other tissues:

Vascular:

  1. cells grow as a benign tumor in epithelium
  2. the cells break through the basal lamina
  3. cells invade the capillary

lymphatic

transcoelomic
Ex: peritoneal or pleural cavities

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10
Q

What are the two theories of tumor formation?

A
  1. clonal evolution
    Develops through repeated rounds of mutations and proliferation
    These damaged cells have a growth advantage
  2. Stem cell
    Tumors contain cancer stem cells
    indefinite proliferate growth
    linked, at first, with leukemia’s
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11
Q

What are the two mechanisms of cell death?

A
  1. necrosis- principle outcome of injury

2. apoptosis- regulated cell death

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12
Q

Describe the characteristics of necrosis?

A
  1. cell swelling
  2. damage to PM
  3. random DNA degradation
  4. inflammation
  5. surrounding tissue damage
  6. cell contents released
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13
Q

What are the features of apoptosis?

A
  1. cell shrinkage
  2. PM blebbing
  3. aggregation of chromatin
  4. fragmentation of the nucleus
  5. DNA fragmentation
  6. caspase cascade activation
  7. no inflammation
  8. no tissue damage
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14
Q

Why would a cell die by necrosis?

A
  1. pathological reasons
  2. acute cell injury
  3. unable to maintain homeostasis
  4. loss of PM integrity
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15
Q

Why would a cell die by apoptosis?

A
  1. physiological reasons
  2. genetic reasons
  3. programmed cell death
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16
Q

How can I assess necrosis in a morphological way?

A
  1. Propidium iodide staining
  2. H&E staining
  3. TEM
17
Q

PI staining and necrosis?

A

live cell imaging

PI labels DNA

PI + = leaky/discontinuous PM (necrosis)

18
Q

How H&E staining determine necrosis?

A

Increased eosinophilia:
loss of cytoplasmic DNA
increased denatured proteins

variable nuclear staining:
typical loss of basophilia and loss of nuclear staining

19
Q

How does TEM help determine necrosis?

A

Discontinuous plasma and organelle membranes

20
Q

How can I biochemically determine necrosis?

A

Random DNA degradation

increased levels lactate dehydrogenase (LDH)

21
Q

How can I tell a cell is going through apoptosis?

A
  1. Membrane phosphatidylserine moves from the inner leaflet to the outer leaflet
  2. The membrane blebs
  3. condensed chromatin is found in the nucleus
  4. Cytochrome C is released from the mito
22
Q

Apoptosis and the immune system?

A
  1. phosphatidylserine is exposed on the surface of apoptotic cells
  2. The apoptotic cell is engulfed or phagocytosed by a macrophage
  3. the engulfed apoptotic cell is internalized then degraded
  4. The macrophage releases cytokines IL-10 and TGF-beta to inhibit inflammation
23
Q

When is apoptosis normal?

A

The development of digits during embryological development

normal tissue homeostasis
billions of cells undergo apoptosis daily, but they are all replaced

24
Q

When is apoptosis abnormal?

A

Loss of cells due to apoptosis

losing irreplaceable cells

accumulation of cells due to the failure of apoptosis

25
Q

What are the two main pathways of apoptosis?

A
  1. intrinsic

2. extrinsic

26
Q

How are intrinsic and extrinsic the same and different?

A

Differ in introduction and regulation

Both result in activation of initiator and executioner caspases

27
Q

Describe the intrinsic pathway of apoptosis?

A
  1. Apoptotic stimulus
  2. The release of cytochrome C
  3. Activation of Apaf1
  4. assembly of apoptosome
  5. Recruitment and activation of procaspase-9
  6. Activation of executioner procaspases
  7. caspase cascade leads to apoptosis
28
Q

Describe the extrinsic pathway of apoptosis?

A
  1. Binding of the fas ligand to the death receptor
  2. recruitment of death domain adaptor protiens FADD and TRADD
  3. the formation of the death inducing signaling complex (DISC)
  4. caspase cascade

activation of initiator caspases (caspase 8)
activation of effector (executioner) caspases (caspase 3)

29
Q

What are caspases and what do they do?

A

They are a family of enzymes that break down proteins

they are synthesized as inactive precursor- procaspases

activated by proteolytic cleavage

30
Q

What is the Bcl-2 family?

A

They are intracellular regulators of apoptosis

Two classes

31
Q

What are the two classes of Bcl-2?

A
  1. pro-apoptotic
    Bid….. links extrinsic and intrinsic pathways

Bax and Bak…….. permeabilization of mitochondrial outer membrane

  1. anti-apoptotic

Bcl-2

32
Q

Pro survival proteins (bcl-2)?

A

bcl-2 and bcl-xL

33
Q

pro death proteins (bcl-2)?

A

Bax
Bak
Bid

34
Q

Bcl-2 family pathway?

A
  1. death receptor signaling results in the activation of caspase 8
  2. caspase 8 cleaves Bid and tBid
  3. Bak and Bax can now enter the mito membrane
  4. cytochrome C is released from the mito
  5. caspases are activated and induce apoptosis
35
Q

Assessment of apoptosis?

A
  1. Caspase activity
  2. Annexin 5- binds to phosphatidylserine
  3. DNA laddering
  4. TUNEL- detects DNA fragmentation

Test 1 FTM (35 decks)

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