PATUM (K2)

2: INTRACELLULAR & EXTRACELLULAR SEDIMENTATION

Fatty ∆ / Lipidosis
ꝱ accumulation of any lipid (cholesterol, 3’gly, phospholipid) within intracellular matrix
• Test using sudan black
• Extracellular lipd accumulation = steatosis
• Fatty tiss inflammation = steatitis
• Serous atrophy = fatty tiss myxomatous degeneration
o Coronary groove: common in cachexia (weakness) → etiologic agent (parasite)
o Normal marrow in young = firm & red brown => active hematopoiesis
o Marrow in adults = firm & white
• Serous atrophy of renal fat
Abnormalities of Lipid Metabolic Pathway
1. excess delivery of free FA: starvation; diabetes mellitus
2. ↑ formation of lipid: toxin shunt FA into 3’gly
3. ↓ production of apoprotein needed forming VLDL: hypoproteinemia. CCl4 poisoning

Glycogen Deposit

• → abnormal glucose metabolism / abnormal glycogen metabolism

• Glycogen: branched polymer of glucose molecules, storage fr glucose
• Normal major deposits occur in liver, muscle & kidney
• Clear vacuoles within cytoplasm / affected cell nucleus
• Periodic Acid Schiff (PAS) stain used to diff glycogen with water ‘/ fat. | Glycogen (+) PAS
Factors:
1. Hyperglycemia (Diabetes mellitus)
2. Drug-induced metabolic disease w disturbed carb metabolism (corticosteroid)
3. Enzymatic deficiencies ass hereditary glycogen storage disease
4. Glycogen-storing ‘clear cell’ hepatocellular tumors

Lysosome Storage Disease / Storage Disease

• Deficiency if lysosomal enzymes involve in synthesis or catabolism of cellular substances i.e.,

glycogen, carb & lipid
• → genetic defects, waste x disposed
• Slow down workflow, substrate x moving thru lysosome
• Symptoms: pain, neurologic damages & shortened lifespan
Enzyme deficiency Substrate acc Disease
a-1,4-glucosidase Glycogen Pompe’s disease
a-1,6-glucosidae Glycogen Cori’s disease
a-L-iduronidase Heparan sulphate Hurler’s Syndrome
L-iduronosulphate sulphatase Dermatan sulphate (Mucopolisaccarids)
Hexosaminidase A GM2 – ganglioside (lipid) Tay Sach’s disease
Hexosaminidase A & B GM2 – ganglioside & globoside (Lipid) Sandhoff’s disease

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PATUM (K2)

Glucocerebrosidase Glucocerebroside (Glycolipid) Gaucher’s disease

a-galactosidase Ceramide trihexosidase (Glycolipid) Fahry’s disease

Intracellular Protein Acc / Protein Inclusion Bodies

Protein deposits:
Absorptive protein • ↑ phagolysosome act
• Hyaline droplet & hyaline droplets of renal tubule
Secretory protein • Protein syn exceeds capacity for release of protein from cell
• Acc of a-1-antitrypsin in liver
Toxic injury Abnormal protein aggregation
Viral inclusion • @ viral replication, new virion aggregates various peptides & other
bodies excess components acc as inclusion bodies
• Bohlinger bodies of Pox virus
• Herpesvirus intranuclear inclusion bodies, Avian ILT
• Morbillivirus intranuclear & cytoplasmic inclusion bodies
• Distemper dog
• Purkinje cell w Negri body
Protein aggregation • Protein polymerize & aggregation disorder → enyme deficiency /
disorder aging
• Transmissible spongiform encephalopathy
• Bovine Spongiform encephalopathy
• Neurofibrillary Tangles
Tau protein
• Alzheimer disease

Amyloidosis

• Clinical state refers to deposition of amyloid material within the body (local or systemic)
• Compose of glycoprotein mass (glycosaminoglycan + protein from fibrin / collagen / globulin)
• Stain brown w iodine
• Amyloid = starch like
• Sago spleen
• Liver amyloidosis
• Stain w congo red + bipolarized microscope

Amyloid type Precursor Occurs in

AA Serum Amyloid A Sepsis
AL Ig Light Chain Plasmacytoma
AI Apolipoprotein Intimal Arteries Pulmonary arteries
IAPP Islet Amyloid Polypeptide Pancreatic islet
Senile B Protein Brain aged animal

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PATUM (K2)

Pathologic Calcification (Mineralized)

Dystrophic calcification
 Calcification of injured cell / areas of necrosis
(coagulative /liquefactive / caseous)
 White muscle disease (nutritional myopathy)
ass w Vit E / Se deficient in farm animals
 Tuberculosis nodules, abdominal fat necrosis
 Microscopically:
▪ Intracellular / extracellular, amorphous,
basophilic granular deposits
▪ Stains black w Von Kossa special stain
Metastatic calcification
 Ca2+ sedimentation → hypercalcemia /
altered Ca2+ metabolism
 Occurrence:
▪ 1° hyperparathyroidism
▪ 2° hyperparathyroidism (renal failure,
nutritional)
▪ Hypervitaminosis D (iatrogenic / plant
analogues)
▪ Paraneoplastic syndrome (c
▪ K9 apocrine gl, adenocarcinoma of
anal sac, k9 lymphosarcoma
 Grossly: white, irregular area, sometimes dry
& gritty
 Intimal artery calcification, alveolar septum
capillary, lumen tubule Ca2+ sedimentation,
gastric mucosa calcification, gastric mucosa
Ca2+ sedimentation

Calcified Bodies

• Calculi: abnormal extracellular masses, composed of Ca & mineral salts dev in organ
Salivary gl Calculus
Intestinal Enterolith
Dental Plaques
Biliary Gallstone
Bladder Cystolith

• Corpora amylacea: large, laminar, round bodies of diverse origin & ass w secretory processes.
• Psammoma Bodies: giant laminated calcified bodies. Present especially in superficial cortex in
meningiomatosis case

Pigment Sedimentation
Endogenous pigment Exogenous pigment

• Ceroid lipofuscin • Carbon pigment: antracosis;

• Melanin pneumoconiosis
• Hemosiderin • Tattoo pigment: Indian ink; Prussian
• Bilirubin blue
• Acid hematin • Secretory pigment from lung lice
Pneumonyssus Simicola

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PATUM (K2)
Ceroid – lipofuscin
• Origin: lipds breakdown, derived from cell
memb (lipid peroxidation)
• “Wear-and-tear” / “aging” pigment
• Sites: aged cells: myocardial cells,
hepatocytes & neurons of old people /
animals / chronically injured cells
• Grossly: yellow-brown discoloration tiss in
severe case (lipofuscinosis)
• Microscopically: golden brown, finely
granular, intracellular pigment
• Significance: x injure cell, sign of aging /
excess free radical damage
• Hepatocyte & cardio
Hemosiderin
• Origin: stored iron (Fe3+), from Hb of
destroyed RBC.
• Fe bound to apoferritin forming ferritin,
excess ferritin form hemosiderin granules
• Sites: normal in macrophages of spleen &
bone marrow. Excessive breakdown of RBC /
excessive acc of iron.
• Areas of congestion / hemorrhage (bruise),
Kupffer cells in hemolytic anemia, alveolar
macrophages in congestive heart failure
(heart failure cells)
• Grossly: light brown color to tiss
• Microscopic: yellow-brown, granular,
intracellular pigment (stain + w Prussian
blue)
• Significance: excess acc → x damage to cell
= hemosiderosis
• Hemochromatosis = excess acc → cell
damaged (idiopathic hemochromatosis of
mynahs)
Melanin
• Insoluble, intracellular, brown-black
pigment from tyrosine
• Origin: normal pigment found in epidermis
& eyes cells.
o Inskin: melanocytes (from neural crest
cell) produce melanin granules =>
inject into keratinocytes  skin / hair
coloration & protection form UV light
• Sites: melanin incidentally @ other sites =>
melanosis, e.g., leptomeninges (esp
rumin), intestine, kidney, lung, base of
aorta
• Grossly: melanosis appear as dark
(pigmented) area / normal tiss
• Microscopically: finely granular, brown,
intracellular pigment
Bilirubin
• End products of heme degradation (x iron);
from senescent RBC
• Origin:
o Heme
o Biliverdin (heme oxygenase)
o Unconjugated bilirubin (biliverdin
reductase)
o Binds albumin & transported to liver
o Conjugate to glucuronide (H2O soluble)
o Excreted in bile
• Sites: hepatocytes (intracytoplasmic /
canaliculi) in renal tubular epithelium
(toxic)
• Grossly: blood & tissue produces yellow
discoloration = jaundice / icterus
• Microscopic: green-brown → yellow-brown
granular intracytoplasmic pigment
• Occurrence:
o Prehepatic jaundice: ↑ breakdown of
RBC (hemolytic disease)
o Hepatic jaundice: failure of
conjugation / excretion
o Post hepatic jaundice: obstruction of
bile duct flow
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Acid-Hematin
• Blood + acid = acid hematic (black color)
• Imparts black color to blood in stomach
(gastric ulcers blood + stomach HCl =
melena)
• Histologic tiss artifact: black precipitation on
slide, due to improperly buffered (acidic)
formalin reacting w blood from tiss
• Carbon pigment: antracosis
Crystal Sedimentation
Urates & uric acid
• Dep of uric acid and urates = gout (purin
metabolism disease)
• Birds excrete uric acid, predispose into gout
• Avian gout:
o Visceral gout: urates deposits in
kidney, live, joint & pericardium)
o Articular gout: urates limited in joint
• Crystal urates = tophus (tophi), HE stains
• Sliver impregnation staining: tophus =
brown-black & fluorescence under
fluorescent microscope
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