Dr. Parsa - Cell Injury and cell death Flashcards

1
Q

A normal cell is confined by a range of function and structural flexibility depending on:

A
  1. the cell’s state of metabolism, differentiation, and specialization
  2. the constraints of neighboring cell’s
  3. the availability of metabolic substrates.
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2
Q

Excess physiologic stress/pathologic stimuli beyond the cell’s threshold to maintain normal homeostasis results in ___ ___

A

cell injury. The injured cell can either adapt to a new steady state which would be reversible, or it could die if it can’t adapt it would undergo necrosis or apoptosis.

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3
Q

Adaptations are ___functional and structural responses to more severe physiologic stresses and some pathologic stimuli, which new altered steady states are achieved, allowing the cell to survive and continue to function

A

reversible

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4
Q

what are the adaptative responses of the cells:

A
  1. atrophy: dec in size and function
  2. hypertrophy: increase in size
  3. hyperplasia: increase in number of cells.
  4. metaplasia: change from one cell type to another
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5
Q

Physiological atrophy is common during normal development. What are some examples of this?

A
  1. notochord and thyroglossal duct during fetal dev.

2. uterus dec in size after parturition

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6
Q

what is the pathologic cause of atrophy

A
  1. disuse
  2. loss of innervations
  3. diminished blood supply
  4. inadequate nutrition
  5. loss of endocrine stimulation
  6. aging
  7. pressure
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7
Q

what is the biomechanical mechanism of atrophy?

A
  1. Decreased protein synthesis

2. Increased protein degradation

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8
Q

What is the molecular pathogenesis of atrophy

A
1. ubiquitin proteasome pathway:
nutrient deficiency or disuse activates ubiquitin ligase which attach the small peptide ubiquitin to cellular proteins and target these proteins for degradation in proteasomes. 
2. increased autophagy:
starved cell eats its own components
3. reduction in size of organelle
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9
Q

what is an ex of residual bodies

A

lipofuscin granule. look yellow/brown

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10
Q

what happens if we see group atrophy

A

considered neurogenic atrophy

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11
Q

describe hypertrophy. what is it due to?

A

increase in cell size, but no new cells! Due to increased functional demand or increased synthesis of structural proteins.

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12
Q

what is physiologic hypertrophy stimulated by?

A
  1. hormones; uterus and breasts in pregnancy

2. inc in workload (exercise): skeletal muscle hypertrophy

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13
Q

what is pathologic hypertrophy

A

Inc. workload associated with changes in gene expression

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14
Q

what is molecular pathogenesis of hypertrophy

A
  1. Phosphoinositidide 3-kinase/Akt pathway

2. Signaling downstream of G protein coupled receptors

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15
Q

Describe physiologic hypertrophy

A
  1. mechanical sensors: triggers for physiologic hypertrophy

2. phosphoinositide 3 kinase/Akt pathway

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16
Q

describe pathologic hypertrophy

A

G protein receptors:

  1. growth factors: TGF, IGF-1
  2. Vasoactive agents: adrenergic agonists, angiotensin II
17
Q

Describe physiological hypertrophy of cardiac muscle

A

sarcomeres are added in series to lengthen the cell, as on periphery to inc width of the cell

18
Q

describe pathological cardiac hypertrophy

A
  1. can produce concentric hypertrophy in which the ventricular wall and septum thicken with a net dec. in ventricular chamber dimensions.
  2. eccentric and dilatory cardiac growth; sarcomeres are added in series to ind. myocytes
19
Q

describe physiologic hyperplasia

A
  1. hormonal: female breast during puberty and during pregnancy
  2. compensatory: liver after partial hepatectomy
20
Q

describe pathologic hyperplasia

A
  1. excessive hormonal stimulation; prostate, endometrium
  2. effects of growth factors on target cells; repair: fibrovascular proliferation
  3. viruses (HPV): epithelial/epidermal proliferative lesions.
21
Q

At the subcellular level, an organelle can undergoe ____ hyperplasia such as _____ hyperplasia in muscle hypertrophy

A

selective; mitochondrial

22
Q

Hypertrophy of the smooth ER is a ____response that inc. the amount of enzymes, _____available to detoxify the drugs.

A

adaptative; cytochrome P-450 oxidase

-overtime patients respond less to the drug bc of this adaptation

23
Q

Which type of hyperplasia is not precancerous

A

BPH (in prostate)

24
Q

what is the most common epithelial metaplasia

A

columnar to squamous

25
Q

in _____it is opposite and changes from squamous to columnar

A

esophagus

26
Q

what are the types of cell injury?

A
  1. reversible

2. irreversible

27
Q

cell injury can occur due to the following cellular functions or components

A
  1. Dec in ATP
  2. Mitochondrial damage
  3. Entry of Ca++
  4. Inc of ROS
  5. Membrane damage
  6. Protein misfolding, DNA damage
28
Q

what are the sequence of events in cell injury

A
  1. biochemical (functional

2. morphologic (structural)

29
Q

what are two features of reversible cell injury

A
  1. cellular swelling

2. fatty change

30
Q

what are features of a irreversible cell injury

A
  1. denaturation of intracellular proteins

2. enzymatic digestion of the lethally injured cell.

31
Q

what is mechanism of apoptosis

A
  1. release of cytochrome c

2. Bcl family of proteins (20) regulate apoptosis