Lecture 03 - Intracellular Accumulation

Question 1

Intracellular Accumulation

Answer 1

1. Fat
2. Protein
3. Pigment

Question 2

1. Fat Accumulation

Answer 2

• gall bladder stone –> lipophage
  1. female
  2. fat
  3. forty
  4. fertile

Question 3

2. Protein Accumulation

Answer 3

intracellular sediments of proteins –> damage to microfilament and microtubules –> mallory body

• alcoholism
• Ig accumulation –> russel body

Question 4

3. Pigments Accumulation

Answer 4

1. Exogenous:
   - anthracotic macrophage: dust endocytosis of macrophages
2. Endogenous:
   - lipofuschin/autophagic vacuole/myelin figure: as a result of degeneration of old organelles
   - melanocytes
   - cholestasis: as a result of obstructive jaundice
   Green pigmentation of liver
   - hemosiderin: non-soluble form of Fe with protein in macrophahes –> hemosiderphage –> hemosiderosis:
3. Localized: after hemorrhages
4. Systemic: accumulation of hemosiderin in a specific organ –> thalassemia
   Golden pigmentation of liver
   –> hemochromatosis

Question 5

Fe Destiny

Answer 5

Fe2+, Fe3+ eaten –> Fe3+ turns to Fe2+ by HCl –> absorption of Fe2+ –> Fe2+ turns to Fe3+ –> attaches to apoferitine (then feritine) or transferine (in liver then to BM) –> used by erythroblast as Fe2+

Question 6

Calcification

Answer 6

1. Dystrophic Calcification

2. Metastatic Calcification

Question 7

1. Dystrophic Calcification

Answer 7

In basic environment of old and necrosis tissues

- old TB necrosis lung tissues can get calcified

Question 8

2. Metastatic Calcification

Answer 8

1. Primary:
   - malignant tumor of parathyroids
   - Excessive PTH1
2. Secondary:
   - kidney: chronic inefficacy of kidney, H+ is secreted
   - lungs: through exhalation CO2 (acid) is lost then OH- remains then Ca(OH)2 is formed
   - stomach: acid is secreted then OH- remains to form Ca(OH)2

Question 9

Cellular Aging

Answer 9

1. Genetic Factors
   - DNA repairs –> accumulation of mutation
   - Genetic abnormalities –> abnormal cellular signaling
2. Environmental Factors –> accumulation of damaged proteins and organelles
   - Free radicals
   - Reduced proteosomal activity
3. Replicative senescence (RNA Template Template Telomerase) –> reduced ability to produce new cells