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pathology > Cell injury (Intracellular Accumulations // Pigments // Pathologic Calcification // Cell Aging) > Flashcards

Cell injury (Intracellular Accumulations // Pigments // Pathologic Calcification // Cell Aging) Flashcards

1
Q

Decsribe Intracellular Accumulation ?

A

Accumulation of substances in abnormal quantities inside the cell : cytoplasm (esp: Lysosomes) or nucleus.
Mild IA => reversible cell injury
Severe IA => irreversible cell injury.

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2
Q

Types of Intracellular Accumulation substances ?

A
  1. Lipids
    Triglycerides (Fatty change)
    Cholestrol and cholestryl ester
  2. Proteins
  3. Glycogen
  4. Pigment
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2
Q

Abnormal IA can be divided into 3 gp. EXPLAIN

A

1. Excessive Accumulation of normal cell constituents : **
Lipids (FA, Cholestrol) // Proteins // CARBS.
2. Accumulation of abnormal subsatnces produced by abnormal meatbolsim due to lack of enzymes **: storage disease // inborn errors of metabolism.
**3. **Accumulation of pigments : endogenous (under certain conditions) OR Exogenous (due to lack of enzymatic mechanisms to degrade them or to transport them to other sites )

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3
Q

Describe FC (Fatty change) or steatosis

A

Accumulation of neutral fat (triglycerides) inside the cytoplasm of the parenchymal cells.
Commonest site is liver but it also can happen in heart, kidneys, skeletal muscle.

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4
Q

What’s a Fatty Liver (FL) ?
Its causes ?

A

accumulation of fat in liver as it plays important role in fat metabolism.

Causes:

  1. Hyperlipidemia : fat entering liver cells exceeds the capacity of liver to metabolize it. As in diabetes mellitus, Obesity, congenital Hyperlipidemia.
  2. Alcohol (most common)
  3. Starvation : Protein calorie malnutrition
  4. Chronic illiness : Tuberclosis => endogenous toxin
  5. Hypoxia : anemia // congenital Heart failure
  6. Drusg : steroids // methotrexate.
  7. Hepatotoxins : Carbon Tetrachloride => exogenous toxin.
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5
Q

Lipids enter the liver cell from ………. or ………….

A

Diet // Adipose tissue (lipolysis)

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6
Q

What can cause a defect in fat metabolsim leading to a fatty liver ?

A
  1. Increase FA entering Liver
  2. Increase synthesis of FA by the liver
  3. Decreased oxidation of FA into ketone bodies => more esterification of FA into triglycerides.
  4. Decrease in alpha-Glycerophosphate => decrease esterification of FA into triglycerides.
  5. Decrease synthesis of Lipid Acceptor Protein => decrease in convertion of triglycerides into lipoprotein.
  6. Blocking excecretion of Lipoprotein out into the circulation.
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7
Q

How does the liver normally metabolzie the fat ?

A
  • Normally, as FA enter the liver cell, most of it will be esterified into triglycerides & few will change into cholestrol, Ketone bodies and phospholipids.
  • Intracellular triglycerides will be converted into lipoprotein reuiring the lipid acceptor protein.
  • Excecretion of lipoprotein into the circulation as Plamsa Lipoprotein (LDL, VLDL)
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8
Q

Liver cell damage occurs when ……………..

A

Fat cannot be metabolized in it.

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8
Q

In most FL, It’s one of the mechanisms that occur but in ……………….., it’s all factors.

A

liver injury by chronic Alcoholism

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9
Q

What are morphologic features of FL ?

A

Grossly:
- Enlargment in liver, soft, tense glitering capsule.
- Pale Yellowish and greasy to touch.
Microscopically
- In H & E stain following paraffin technique shows the fat as unstained vacuoles in cytoplasm of hepatocytes as fat is dissolved in alcohol.
- Initially, fat vacuoles are small and present around the nucleus (Microvesicular).
- W/ progression of process, Vacuoles become large pushing the nucleus to the periphery of the cell to be flattened giving the ring appearance. (Macrovesicluar).
- Hepatocytes laden w/ large fat vacuoles may rupture causing these vacuoles to coalesce forming fatty cysts.
- Then, lipogranulomas appear consisitng of collection of lymphocytes, macrophages & some multinucleated giant cells.

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10
Q

What special stains to use to more observe fat ?

A
  1. Sudan dyes (III, IV, sudan Black).
  2. Oil red O
  3. Osmic acid
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11
Q

How does the body regulate cholestrol amount to prevent its accumulation ?
What happens to be accumulated ?

A
  • Most cells use it to synthesize their cell memb.
  • However, under certain pathological conditions, Phagocytic cells filled w/ lipids change into foam cells.
  • Pathological conditions as :
    * Sites of old hermorrages & infarcts : cholestrol is derived from broken RBCs & dead cells.
    * Accumulation of cholestrol in tunica intima in arteries in case of atherosclerosis.
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12
Q
  1. Excess Accumulation of proteins appear in cytoplasm of cell as ………..
  2. I w conditions ?
A
  1. Eosinophilic cytoplasmic droplets.
  2. This can occurs in :
    A. Kidney disorder resulting in heavy protein filtration (Proteinuria) : pinocytosis increases & fuse w/ lysosomes forming pink (eosinophilic) hyaline cytoplasmic droplets in epithelium of proximal convoluted tubule.
    B. Rhinoscleroma : Accumulation of newly synthesized IG in rER in plasma cells cytoplasm as round eosinophilic => Russel bodies
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13
Q

What can cause Glycogen accumulation ?
AND Where ?

A
  1. As in Glycogen stroage disease, the lack of enzymes => abnormal glycogen metabolism=> its accumulation.
  2. In Cardiac M. Fibers, Skeletal M. Fibers, Liver cells w/ secondry tissue injury.
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14
Q

What are pigments ?

A

Colored substances that are either endogenous or exogenous.
Endogenous as : Melanin, Haemoprotein derived pigment (Haemosedrin), Lipofuscin.
Exgenous as : Inhaled pig. (Carbon) // Injected pig (Tattowing)

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15
Q

Describe the melanin ?

A

Brown-black pigment present in Hair, Skin, choroid od eye, Adrenal medulla, meninges.

16
Q

What are Melanin pigmentation disorders ?

A

I. Hyperpigmentation

  1. Generalized :
    - Addison’s disease due to increase in MSH (melanin stimulating hormone) & ACTH (Adrenocorticotropic Hormone).
    - Chloasma during pregnancy, in face / nipples genitalia => as stimulation of melanocytes by female sex hormones : estrogen & Progestrone => more melanin release.

2. localized :
- Freckles : brown skin patches in sun exposed areas.
- Melanotic tumors : Benign as pigmented nevi, and malignant melanoma due to increase melanogenesis.

II. Hypopigmentation :

  1. Generalized :
    Albinism : tyrosinase activity of melanocytes is genetically defective => no melanin is produced.
  2. Localized :
    - Vitiligo
    - Leprosy : as wound healing
17
Q

What can cause excessive Haemosedrin storage ?

A

Increase in RBCs Breakdown or systemic iron overload.

18
Q

Iron is stored in the tissues in 2 froms : ………. & ………..
Describe each form ?

A
  1. Ferritin & Haemosedrin.
  2. Discription :
    I. Ferritin :
    - is iron attached to apoferritin.
    - Soluble
    - NO LM, ONLY EM.

II. Haemosedrin :
- Aggregation of Ferritin.
- Identified by LM as golden yellow to brown granular pigments.
- Normal amounts can be found within mononucleated phagocytes in Liver, spleen, bone marrow where RBCs breakdown taked place.
- Insoluble.
- Special Stain : Perl’s or Prussian Blue Reaction => deep blue granules.

19
Q

Haemosedrin Accumulation can cause : ……. & ……

A

Haemosidrosis & Haemochromatosis

20
Q

Describe Haemosidrosis

def // types

A
  • Deposition of hemosedrin in mononuclear phagocytes w/o causing tissue injury.
    => Localized :
  • Caused by hemorrhage in tissue => breakdown of RBCs => HB degraded and stored in Macrophage as Haemosedrin.
  • EX : IN Chronic Pulmonary Venous Congestion : we can find **Brown induration **resulting from small hemorrhages. & Heart Failure cells w are Haemosedrin-laden alveolar MQ.
  • => Generalized :
    Caused by systemic iron overload due to :
  • Reapeated blodd transfusion or parenteral iro therapy.
  • Chronic Haemolytic Anemia as Thalassemia.
  • Excessive dietary intake of iron.
21
Q

Describe Haemochromatosis ?

A

=> Progressive & more extensive accumulation of Haemosedrin in parenchymal cells throughout the body esp. in Liver, pancreas, heart, endocrine glands with tissue injury.

=> Primary (hereditary)
- caused by excessive intestinal absorption of iron even when the amount taken is normal.
- Autosomal dominant disease ccc by a triad : pigmented liver cirrhosis & pancreas damage => diabetes mellitus & bronze colored skin pigmentation (bronze diabetes)
=> Secondary (Acquired)

  • Long term of generalized Haemosiderosis.
22
Q

Describe Lipofuscin ?

Color, Site

A
  • Yellow to brown intracellular lipid pigm.
  • Found in atrophic cells => “wear & tear pig).
  • Sites : Myocardial fibers (brown atrophy of Heart) / hepatocytes / neurons / Leydig cells in testis.
23
Q

What is Lipofuscin Pathogenesis ?

A

Lipofuscin is a collection of undigested material in lysosome failed to be eliminated after intracellular lipid peroxidation => deposited as lipofuscin pig.

24
Q

What is an exogenous Pig ?

A

A pigment introduced into the body from outside by inhalation // ingestion // inoculation.

25
Q

Describe inhaled pig & Injected ones

A

1. Inhaled pig.
- EX : Anthracosis w means the deposition of carbon particles in tissues.
- After carbon inhalation, carbon is taken up by alveolar MQ, some of MQ are coughed out, some settle in intertitial fluid => to lymphatics => deposisted in Hilar LN.

2. Injected pig.
EX : Tattooing.
- Pig as india ink is introduced in the dermis during the tattooing process => pigm taken up by MQ and remains permenantly in CT.

26
Q

What is Pathologic Calcification ?

DEF // Histologically // Types

A

DEF:
deposition of calcium salts in tissues other than osteoid & enamel => pathologic or heterotopic calcification
Histollogically: Calcium salts appear as deep basophili, irregular, granular clumps.
Occasionally, heterotopic bone formation (ossification) may occur.
Types:
1. Dystrophic
2. Metastatic

27
Q

Describe Dystrophic Calcification

A

it’s ccc by deposition of Ca salts in dead or degenerated tissues w/ normal Ca metabolism & Normal serum Ca level (9-11 mg/dl).

28
Q

Causes of Dystrophic Calcification ?

A

Calc. in dead tissues:
- Fat, coagulative, liquifactive, caseous necrosis
- Haematomas
- Dead parasites as Hydatid cyst & schistosoma eggs

Calc. in degenerated tissues:
- valves oh Ht in old age & rheumatic vavulitis
- Atheroma in aorta and coronaries
- Dense old scars undergo hyaline degeneration & subsequent calcification

29
Q

What is pathogenesis of Dystrophic Calci. ?

A

denaturated proteins from necrotic or degenerated tissues bind phosphate ions and react w/ Ca ions => percipitates of Ca Phosphate.

30
Q

Describe metastatic Calcification

A

it’s ccc by deposition of Ca salts in normal tissues w/ abnormal Ca metabolism & increase serum Ca level (Hypercalcimia)

31
Q

Causes of Metastatic Calcification ?

A

1. Excessive release of Ca from bone
- Hyperparathyrodism
- Bone distructive lesions : multiple myloma & metastatic carcinoma
- Prolonged immobilization of patient => disuse atrophy of bone & hypercalcemia.
2. Excessive absorption of Ca by the gut
- Hypervitaminosis D
- Milk-alkali Syndrome, caused by excessive oral intake of Ca in the from of milk, and administration of calcium carbonate as a treatment of peptic ulcer
3. Vitamin D Disorder
- Vitamin D intoxication
- Sarcoidosis (MQ activating Vit D precursor)

32
Q

What is pathogenesis of Metastatic Calci. ?

A

Excessive binding of inorganic Phosphate ions to excess calcium ions => excessive precipitation of calcium salts

33
Q

What are Sites of Metastatic Calc. ?

A

Any normal tissue but more common in :
1. Kidneys : in basment memb of tubular epi. & tubular lamina causing nephrocalcinosis.
2. Lungs : alveolar walls
3. Stomach: fundic mucosal tissue.
4. Artery : internal elastic lamina
5. Synovium of joint : causing pain & dysfunction

34
Q

Metatstatic calci is reversible if ………..

A

correction of abnormal Ca metabolism

35
Q

Compare betw Metastatic & Dystrophic calcification

DEF // Ca Metabolsim // Ca serum level // Causes // Pathogenesis

A

-1. DEF
DY : deposition of Ca salts in dead or degenerated tissues
ME : deposition of Ca salts in normal tissues

2. Ca Metabolsim
DY: normal
ME: deranged

3. Ca serum level
DY: normal (9-11 mg/dl)
ME: hypercalcimia

4. Causes
DY : Necrosis // Haemoatoma // Dead parasites // Atheroma // old scars // Rheumatic valvulitis
ME : hyperparathyrodism // Bone destructive lesions // Disuse Atrophy of bonse // Hypervitaminosis D // Milk-alkali syndrome // Sarcoidosis.

5. Pathogenesis
DY: denaturated proteins from necrotic or degenerated tissues bind phosphate ions and react w/ Ca ions => percipitates of Ca Phosphate.
ME : Excessive binding of inorganic Phosphate ions to excess calcium ions => excessive precipitation of calcium salts

36
Q

Life expectancy of an individual depends on …….. & ……… &………. &……….
Expain them ?

A
  1. Intrinsic genetic process : Genes controlling responses to endogenous or exogenous factors initating Apoptosis.
  2. Environmental Factors : Diet // consumptio or inhalatio of harmful substances …
  3. Individual Lifestyle : Alcoholism => cirrhosis & hepatocellular carcinoma.
    Drugs addiction
    Smoking => bronchogenic carcinoms & respiratory disease.
  4. Old age disease : Atherosclerosis // Diabetes Mellitus // Ischemic Ht Disease // Hypeetension.
37
Q

What is cellular aging ?

A

it’s the result of progressive decline in proliferative capacity & lifspan of cell and the effects of contineous exposure to exogenous factors => cell damage.

38
Q

What are cellular basis of aging ?

A
  1. Decreased cellular replicatio
    - Every cell has its nb of cell division capable of making, when this nb is done, the cell is arrested & enter the replicative senescent.
    - EX : Fibroblasts can go through 65 doublings b4 entering replicative senescent.
    - This mechanism of limited capacity of repliaction is due to shortening of telomere at tips of chromosome w/ every replication, in normal cells, lost telomere is immediatly replaced by newly synthesized one by telomerase enzyme.
    - With aging, there is inadequate amount of telomerase enzyme => telomere lost w/ replucation cannot be replaced w/ new one => shortening of chromosomes => senescence
  2. Oxidative stress (free readical-mediated injury)
    - W/ aging : low metabolic rate w/ generation of toxic oxygen radicals => failure to eliminate them => accumulation => oxidative damage to mitochondria => cell damage.
    - Antioxidants serve to delay oxidant damage.

pathology (4 decks)

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