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MBLDD Block 3 > Cell Path > Flashcards

Cell Path Flashcards

1
Q

Three groups of macromolecules composing the ECM

A

1) Fibrous structural proteins

collagens and elastins: to provide tensile strength

2) Cell adhesive glycoproteins:

connect matrix elements to one another and to cells

3) Proteoglycans and hyaluronan: provide resilience and lubrication

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2
Q

Types of Intercellular Signaling

A

•Autocrine

–Cell response to self made signals

•Paracrine

–Target cell in close proximity to secreting cell

•Endocrine

–Target organ distant from secreting cell

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3
Q

Major Receptor/Ligand Classes Involved in Cell Growth:

A
  1. Receptors with intrinsic tyrosine kinase activity

Growth factors and insulin, active kinase phosphorylates effector molecules

  1. Receptors without intrinsic tyrosine kinase activity

Recruit kinases: Cytokines, activating JAK (Janus kinase) proteins

  1. Transmembrane G-protein linked receptors

Chemokines, adrenergic agents, activate G proteins/cAMP pathway for multiple effects

  1. Steroid hormone receptors

Located in nucleus and function as ligand dependent transcription factors

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4
Q

HSP definition

A

Heat shock proteins (HSP) are a family of proteins that are produced by cells in response to exposure to stressful conditions

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5
Q

Roles of HSP

A

They participate in the process of protecting newly formed polypeptides from misfolding (chaperones) and help the cell get rid of already misfolded or damaged proteins by binding them to ubiquitin (a low-mol weight HSP) and thus making them targeted for digestion by specific proteases (cellular housekeeping)

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6
Q

What is metaplasia

A

Metaplasia is a reversible change in which one differentiated cell type (epithelial or mesenchymal) is replaced by another cell type as an adaptive response to factors in the microenvironment.

The result of a reprogramming of stem cells that are known to exist in normal tissues, or of undifferentiated mesenchymal cells present in connective tissue

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7
Q

Causes of atrophy

A

Causes of atrophy include a decreased workload (e.g., immobilization of a limb to permit healing of a fracture), loss of innervation, diminished blood supply, inadequate nutrition, loss of endocrine stimulation, and aging (senile atrophy)

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8
Q

Most common mechanisms of intracellular deposits/accumulations

A
  1. Lipids
  2. Excessively produced or aberrant proteins
  3. Glycogen is increased in some inherited enzyme deficiencies
  4. Pigments (can be endogenous or exogenous)
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9
Q

Pathologic calcification def

A

the abnormal tissue (extracellular) deposition of calcium salts, together with smaller amounts of iron, magnesium, and other mineral salts

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10
Q

Dystrophic vs metastatic calcification

A

Dystrophic: in nonviable or dying (necrotic) tissues in the presence of normal calcium serum levels

Metastatic: In norml tissue but in cases of hypercalcemia due to derangement of calcium metabolism

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11
Q

What are neoplastic cells

A

Autonomously growing cell with infinite growth potential. The initial process of transformation is referred to as dysplasia and when a mass is produced it is referred to as neoplasm or new growth

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12
Q

Dysplastic vs hyperplastic cells

A

Dysplastic cells are different from hyperplastic cells mainly in the appearance of their nuclei which become larger and darker (hyperchromatic)

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13
Q

Stages of cell injury

A
  1. Damage to the mitochondria which results in reduced ATP (energy) production
  2. hydropic degeneration - failure of the cell membrane ATP-dependent Na/K pump that maintains water balance across cell membrane which leads to cellular swelling
  3. accumulation of fat droplets and misfolded proteins - inadequate lipid metabolism
  4. Nuclear damage
  5. cell death either by necrosis or apoptosis.
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14
Q

Necrosis vs apoptosis

A

Necrosis - usually many cells are involved simultaneously and cell death is associated with disruption of cell membrane and leakage of intracellular molecules that induce an inflammatory reaction

Apoptosis - single cells are involved and the cell membrane remains relatively intact until the whole dead cell body is phagocytized , thus no inflammatory reaction is elicited

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15
Q

What cell signal molecules allow for apoptosis

A

Cytochorme C from mitochondria and caspases

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16
Q

Distinguishing factors of necroptosis

A
  • involvement of receptor associated kinase 1 and 3 (RIP1 and RIP3)
  • No involvment of caspases
  • the terminal events include permeabilization of lysosomal membranes, generation of free radicals, damage to the mitochondria, and reduction of ATP levels
17
Q

Distinguishing factors of pyroptosis

A
  • occurs in cells infected by microbes
  • Incolves caspase 1 and 11
  • characterized by swelling of cells, loss of plasma membrane integrity, and release of inflammatory mediators
18
Q

karyopyknosis

A

shrinkage with chromatin aggregation=dark color

19
Q

karyorrhexis

A

Breakdown or fragmentation

20
Q

karyolysis

A

Dissolution or disappearance of nucleus

21
Q

liquefactive necrosis

A

inflammatory cell enzymes liquefy the dead tissue and later macrophages remove the dead cells and debris, leaving a cystic area that forms in the region of infarction

22
Q

Types of autophagy

A

1- Chaperone-mediated autophagy (direct translocation across the lysosomal membrane by chaperone proteins)

2- Microautophagy (inward invagination of lysosomal membrane for delivery)

3- Macroautophagy

23
Q

Steps of autophagy

A

initiation (LC3 involved), nucleation, and elongation of isolation membrane

24
Q

Causes of cellular aging

A
25
Q

Function of sirtuins

A

Sirtuins are a family of NAD-dependent protein deacylases

Sirtuins are thought to promote the expression of several genes whose products increase longevity. These include proteins that inhibit metabolic activity, reduce apoptosis, stimulate protein folding, and inhibit the harmful effects of oxygen free radicals

26
Q

Labile Cells

A
27
Q

Quiescent (stable) cells

A
28
Q

Nondividing (permanent) cells

A
29
Q

Size of cell population is determined by:

A
  1. Rate of proliferation
    - Physiologic
    - Pathologic
  2. Differentiation

Types of cells

  1. Death by apoptosis
30
Q

Life cycle of stem cells (6 steps starting w zygote)

A
31
Q

Source and function of stem cells

A

Stem cells are essential to tissue regeneration and repair

In all labile & quiescent tissues

Patient-specific pluripotent stem cells can be induced in vitro by adding stem-cell genes (Sox-2; c-Myc etc) to cultured diff cells

32
Q

Contact inhibition

A

Cells capable of dividing cease proliferation as they become in contact with other cells

33
Q

Process of cellular repair bny fibrosis

A

Persistent tissue injury leads to chronic inflammation and loss of tissue architecture. Cytokines produced by macrophages and other leukocytes stimulate the migration and proliferation of fibroblasts and myofibroblasts and the deposition of collagen and other extracellular matrix proteins. The net result is replacement of normal tissue by fibrosis

34
Q

Phases of scar formation

A
  • Inflammation: neutrophils and macrophages phagocytizing and cleaning the debris with formation of blood clot
  • Proliferation of repair cells: Angiogenesis, Migration and proliferation of fibroblasts, re-epithelialization of surface
  • Maturation: ECM deposition, tissue remodeling, wound contraction
35
Q

Healing by primary vs secondary intention

A
36
Q

Angiogenesis from EPCs and pre-existing vessels

A
37
Q

Wound strength soon after injury and later

A
38
Q

Keloids

A

scar tissue grows excessively, forming smooth, hard growths called hypertrophic scars or keloids

39
Q

Contractures

A

Deformities around the joints may take place when mature scars retract

MBLDD Block 3 (8 decks)

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