First Lecture Flashcards

Cell injury (20 cards)

1
Q

Causes of cellular injuries

A
1. Hypoxia – Ischemia
2. Physical Agents
3. Chemical Agents & Drugs
4. Infectious Agents
 5. Immunologic Reactions 
6. Genetic derangement 
7. Nutritional Imbalance 
8.Ageing
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2
Q

Main reasons for hypoxia_ischemia

A

A- Atherosclerosis & Thrombi
B- Cardiopulmonary failure
C- Loss of oxygen carrying capacity, e.g. pneumonia, anemia, CO poisoning

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3
Q

Physical Agents that cause cell injuries

A
A- Mechanical trauma 
B- Extremes of temperatures 
C- Sudden change in atmospheric pressure 
D- Radiation 
E- Electric Shock
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4
Q

Example of Chemical Agents & Drugs that may causes a cell injury

A
A-Glucose and salts 
B-Oxygen 
C- Heavy Metals 
D- Insecticides 
E- Ethanol
 F-Carbon Monoxide
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5
Q

Physiologic Cellular Adaptation to Injury

A

Normal stimulation by hormones, e.g. enlargement of breasts in pregnancy and lactation

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6
Q

Pathologic Cellular Adaptation to Injury

A
  1. Atrophy
  2. Hypertrophy
  3. Hyperplasia
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7
Q

Atrophy defenition

A

Shrinkage in the size of the cell due to loss of cell substance -> diminished function

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8
Q

Causes of atrophy

A
  1. Decreased workload
  2. Loss of innervation
  3. Decreased blood supply
  4. Inadequate nutrition
  5. Loss of endocrine stimulation
  6. Ageing
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9
Q

What is the Autophagy

A

starved cell eats its own components to find nutrients

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10
Q

Cells contain 2 proteolytic systems (enzymes) that result in protein degradation

A

1- Lysosomes

2- Ubiquitin

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11
Q

The degradation of cellular proteins occurs mainly be the

A

ubiquitin-proteasome pathway

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12
Q

What cause activate ubiquitin ligases, and what does it do

A

Nutrient deficiency and disuse may activate ubiquitin ligases, which attach multiple copies of the small peptide ubiquitin to cellular proteins and target these proteins for degradation in proteasomes.

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13
Q

Hypertrophy mean

A

It is an increase in the size of cells and with such change, an increase in the size of the organ.
- More structural component

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14
Q

Example of physiological hypertrophy

A

The uterus during pregnancy, Muscle building.

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15
Q

Example of pathological hypertrophy

A

Cardiac hypertrophy in hypertension and cardiac valve diseases.

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16
Q

The result of atrophy

A

Decrease in the structural component of the cell. Imbalance between protein synthesis and degradation, .i.e. Decreased synthesis, Increased degradation, or both
Autophagy : starved cell eats its own components to find nutrients

17
Q

The result of hypertrophy

A

1- The synthesis of more proteins and myofilaments per cell.
2- There may also be a switch of contractile proteins from adult to fetal or neonatal forms.(during muscle hypertrophy, the α-myosin heavy chain is replaced by the β form of the myosin heavy chain, which has a slower, more energetically economical contraction.)

18
Q

Hyperplasia mean

A

It is an increase in the number of cells in an organ or tissue

19
Q

Cells are divided into 3 types depending on their ability to divide

A

1- Cells with high capacity for hyperplastic growth (labile cells)
e.g. hematopoietic cells in bone marrow, epidermis, intestinal epithelium, exocrine duct epithelia, and transitional epithelia of the urinary bladder.
2- Cells with low capacity (permanent cells)
E.g. Nerves and cardiac muscle cells
3- Cells with intermediate capacity (stable cells)
E.g. Cartilage and smooth muscle cells

20
Q

Hyperplasia can be divided into

A

1- Physiologic : A. Hormonal hyperplasia (breast, uterus) B. Compensatory hyperplasia (liver) 2- Pathologic : A. Excessive hormonal stimulation (endometrial hyperplasia) B. Effects of growth factors on target cells. (Stimulation by growth factors, wound healing, viral infections