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Pathology > Intercellular Accumulations > Flashcards

Intercellular Accumulations Flashcards

1
Q

4 main types of accumulation pathways

A

1 ingestion of exogenous subs - with not way of dealing with them

2 accumulation of endogenous substrates - which can’t be degraded ( pigments )

3 abnormal metabolism ( glucose, lipids proteins )

4 defect in protein folding - accumulation of defected proteins

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2
Q

List the type of pigment accumulation ( both Endo and exogenous)

A 
1 melanin 
2 lipofuschin
3 hemosiderin 
4 coal dust 
5 tatoo deposits
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3
Q

How is melanin made

Is melanin the only endogenous black brown pigment

What does melanin do

A
  • tyrosinase enzyme catalyzes oxidation of precursor tyrosine to dihydroxyphenylalanine in melanocytes
  • yes
  • gives color to skin , hair , brain ( substatia nigra)
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4
Q

What is the special stain for melanin and the color for positivity

A

-massona fonta. ( black )

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5
Q

How is Fe transferred and stored in body

Outcome of excess stored Fe

A

-transferretin proteins transfer Fe

/stored with apoferritin to form ferritin miecelles

-Excess Fe causes excess ferritin miecelles which aggregate to form hemosiderin

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6
Q

Where are hemosiderins mainly seen inside the body and why

A
  • liver, bone marrow , spleen

- sites of RBC breakdown

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7
Q

How do bruises acquire hemosiderins and the other changes that occur

A
  • at site of Bruise injured RBC r phagocytized to recover Fe. Which is incorporated in apoferritin-ferritin miecelles - hemosiderin
  • heme group is converted to biliverdin ( green bile ) and then bilirubin ( red bile ). Causes color change of a bruise
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8
Q

How does local overload of Fe occur and systematic

What is hemosiderosis

A

-during hemorrhaging

  • increases Fe absorption due to metabolism error ( hemochromatosis )
  • hemolytic anemia’s : premature lysis of RBC
  • repeated blood transfusions

-accumulation of Fe in numerous organs due to overload systematic overload of Fe

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9
Q

Colour and characteristic description of Fe under microscope

Special stain for Fe and colour for positivity

A
  • golden yellow
  • refractive

-Perls stain , Prussian blue stain ( hemosiderin will be blue )

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10
Q

How is lipofuschin formed and its components

Why does lipofuschin form !?

A
  • perioxidation of cellular lipids by lysosomes
  • complex of lipids and proteins
  • as people age cell damage occurs more frequently and lipids peroxidized
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11
Q

What does accumulation of lipofuschin show

Colour in light M/S

Characteristic location of lipofuschin

Special stains for lipofuschin

A
  • tell tale sign of free radical damage
  • yellow brown in light M/S
  • peri nuclear
  • osmium tetraoxide , oil red o , Sudan black b
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12
Q

Causes of lipofuschin and where seen

A
  • prominent in heart and liver of aging patient
  • cancer cachexia
  • severe malnutrition
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13
Q

Describe how coal dust accumulates and why

Where seen

What is anthracosis

A
  • when carbon is inhaled macrophages in lungs engulf but have no mechanism to deal with the coal dust
  • so keep the dust
  • in lungs and at lymph nodes
  • blackening of tissue due to aggregates of macrophages with coal dust trapped
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14
Q

How is coal workers pneumoconiosis formed

A

-coal miners inhale coal dust which induces emphysema and causes the disease at hand

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15
Q

How do tattoos cause pigment accumulation and effects

A
  • the ink is engulfed by macrophages at all dermis levels and they have no way of dealing with it so kept
  • tattoos permanent for the remainder of the embellished life
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16
Q

What is the most common accumulated lipid , where mostly seen and why

Effect of lipid trapped in heart

A
  • TRIG. Seen mostly in liver as it is sight of major lipid metabolism
  • Tigered effect , tabby coat appearance ( alternating red / brown color of heart and yellow deposits of lipids )
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17
Q

Special stains of lipids and brown colors for positivity

What is frozen section
We used and which stain is used on it

A

1 oil red o - red
2 Sudan black - black
3 osmium tetroxide

  • fresh untreated tissue
  • treating sample might degrade some components
  • oil red o
18
Q

What is steatosis

List the major causes of fatty exchange and describe them

A
  • abnormal accumulation of lipid in cells ( TRIG )
  • protein malnutrition : reduces apoprotein levels and TRIG not converted into lipoprotein
  • anoxia : reduced O2 and TRIG can’t be oxidized causing steatosis
  • alcohol : inhibits sER and mito functioning and TRIG not converted into phospholipids or oxidized
19
Q

Briefly describe lipid metabolism

A
  • lipids catabolized in GIT to form free fatty acids wc r introduced into liver
  • FA anabolized into TRIG which is then converted into lipoproteins, cholesterol, phospholipids and oxidized into acetone , acetonic acid
20
Q

Describe how foamy cells are formed

A

-excess cholesterol is phagocytized by macrophages and the chol accumulates as vacuoles in cell which look foamy

21
Q

Describe atherosclerosis formation and appearance

Describe xanthoma formation

A
  • smooth muscle Cells in arterial initima are filled with lipid vacuoles with chol and chol esters
  • cells have a foamy appearance

/intercellular accumulation of lipids in macrophages and the clusters form tumor masses called xanthoma

22
Q

What is cholesterolosis

A

-accumulation of cholesterol laden macrophages in Lamina propia of gallbladder

23
Q

What is Niemann-Pick disease how it occurs

A

-lysosomal storage disease where there is an error in cholesterol metabolism and cholesterol is stored in multiple organs

24
Q

Structure and appearance of protein accumulations

A
  • rounded eosinophilic vacuoles in cyto

- can be crystalline or amorphous

25
Q

Describe reabsorption of proteins in proximal renal tubes

A
  • there is protein ( proteinuria) loss in urine through glomerulus
  • proteins now rearbsorped increasing cellular conc
26
Q

What is diabetes mellitus and its cause

What does Uv light to melanocytes

A
  • abnormal metabolism of glucose and it is stored in cells

- production of melanin

27
Q

How does Mallory hyaline body come about

A
  • excess alcohol causes liver cells to assume that there is an excess cytoskeleton
  • cytoskeleton degraded by it immediately grows back in larger amounts in and there is accumulation of cytokeratin 8 and 18
28
Q

How does multiple myeloma come about and where is it accumulation

A

-tumor in plasma cells causes overproduction of immunoglobulin and it accumulates in cell as Russel body ( Cyto ) and Dutchers body ( nucleus )

29
Q

How do misfolded proteins accumulate and some associated diseases

What is proteopathy

A
  • defect in chaperones and defect proteins Accumulate
  • Alzheimer’s
  • Parkinson’s
  • Huntington

-proteopathy is accumulation of mis folded proteins affecting normal functioning

30
Q

Where do xanthoma’s form

Characteristic feature of atherosclerosis

A
  • near the skin

- yellow pigment

31
Q

What is hyaline change

A

/alteration in or out of cell to give a homogeneous glass pink appearance with H and E stain due to accumulations

32
Q

How to test and confirm presence of glycogen and positivity color

A
  • PAS test pink for positive ( per-iodic acid schiff )

- diastase test to confirm. Glycogen hydrolyzed and positive PAS color gone

33
Q

What is glucogenoses

Where does glycogen accumulate !?

A

-accumulation of glycogen due to abnormal metabolism

  • beta cells of islets of Langerhans
  • liver
  • heart muscle cells
34
Q

What is pathological calcification

Types and differentiate them

A

-abnormal accumulation of Ca salts other than osteoid of enamel

1 dystrophic - Seem In dead and dying tissue
-has normal Ca2 levels

2 metastatic - seen in healthy tissue
-has elevated Ca Levels

35
Q

Where is dystropic calcification seen

Examples of where dead calcification is seen

A

-in fat , liquifactive and Caseous necrosis

  • Gamna Gandy bodies
  • hematoma
  • dead parasite
  • venous thrombosis
36
Q

Examples where dying calcification is seen

A
  • psammoma body : calcification of tumors in lamina concentric fashion resembling grains of sand
  • senile degenerative calcification
  • anthema
  • Monkerberg medial calcification
  • calcinosis cutis
37
Q

4 causes of hypercalcemia

A
  • increased Ca absorption in intestines
    1 bone lesions
    2 extend bed rest ( disuse atrophy of bone )

-increased bone resorption
1 hyperparathyrotism due to tumor or parathyroid hyperplasia

  • renal failure: will keep numerous phosphates and Ca has to rise to increase balance
  • excess vitamin D ( hypervitaminoses )
38
Q

What is sarcoidosis

A

-activation of vitamin D precursor by macrophages

39
Q

Describe pathogenesis of calcification in dystrophic

A
  • Ca binds to membrane of cells
  • phosphatase is released and it produces phosphate
  • P binds to C and calcium hydroxyapatite crystals are formed
  • crystals grow fuse and form calcium deposits
40
Q

Where is psammoma body found and causes ( 1st 4 letters )

A

-necrotic tissue

  • papillary carcinoma of thyroid
  • somatose tatinoma
  • mengioma mesothelioma

Pathology (13 decks)

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