i want 25 multiple choice questions with their model answer below each question the covers different aspects of all of the following information: Apoptosis
➢ Second type of cell death defined as death of single cells within clusters of other cells.
➢ Referred to programmed cell death.
➢ It is an important mechanism for the removal of unwanted cells as occurs in cells with unrepaired DNA damage protecting against neoplastic transformation.
➢ Physiological or pathological.Mechanism of apoptosis
1. Cell shrinkage, loss of microvilli and cell junctions. 2. Regular fragmentation of DNA. 3. Membrane bleeping. 4. Formation of apoptotic bodies. 5. Rapid phagocytosis of apoptotic bodies. 6. Absence of surrounding inflammation (why??).Feature
Cellsize
Nucleus
Difference between necrosis and apoptosis
Necrosis
Apoptosis
Enlarged(swelling)
Pyknosis → karyorrhexis
→karyolysis
Plasmamembrane Disrupted
Cellularcontents
inflammation
Cause
Enzymatic digestion; may
leakout ofcell
Frequent
Invariably pathologic
Reduced(shrinkage)
Fragmentation
into
nucleosome-size
fragments
Intact
Intact
No
Often physiologicIntracellular accumulation
Substances may accumulate in the cells
 Water
 Fat
 Mucin
 Glycogen
 Protein
 PigmentsHyalinosis
Hyalinosis means the deposition of a glassy, homogeneous, structurless
eosinophilic protein substance either inside cells or in connective tissue.
Intracellular haylinosis :
Mallory hyaline chronic alcoholic liver
Corpora amylacia prostate
Russell bodies plasma cell in Rhinoscleroma
Old thrombus
Zenker Degeneration or necrosis: in skeletal muscles (rectus muscle and
diaphragm) after typhoid fever infection.
Connective tissue hyalinosis (Extracellular):
1- Wall of blood vessels (arterioles and capillaries) in chronic hypertension.
2- Old scars, tumors.Grossly: swollen, pale, soft, friable
hemorrhagic mass.
Microscopic: swollen cells with
structureless homogenous red materialMucoid change
 Excess mucin in cell
 Signet ring appearance in
carcinoma of the stomach.
 Catarrhal rhinitisDef.:
Pathogenesis:
Grosspicture:
Increased size and weight Soft in consistency and pale color
with tense capsule
Microscopicpicture: Cytomegaly and pale
eosinophilic vacuolated
cytoplasm/ nucleus appear normal
Examples:
-Viral hepatitis
- Diabetes mellitus
- Epidermal cells in burns, Herpes
Simplex & Zoster.
- Renal tubulesPigment
Endogenous
Melanin
Exogenous
Lipofuscin
Hemoglobin derived
Inhalation
Ingestion
InoculationPathological pigmentation
Pigments are colored substances that stain the tissue
Endogenous pigments Lipofuscin Melanin Bilirubin
Hemosiderin.
Exogenous pigments Tattoo, anthracosis, lead poison.
Hemoglobin derived pigments
➢ Bilirubin
➢ Hemosiderin
➢ Hematin➢ Melanin: It forms the normal color of skin, hair, iris & parts of
CNS. It is Sulphur containing pigments & appear as pale yellow
to deep brown.
➢ Examples of increased melanin pigments:
Prolonged exposure to sun: due to stimulation of MSH
Pregnancy , Tumors: Melanoma, Chronic irritation.
➢ Examples of decreased melanin pigments: Albinism: partial or
complete absence melanin from skin, hair, or iris.Hemosiderin
Hemoglobin derived pigments: RBCs at the end-of-life span releases its HB content which is then
metabolized into: globulin and haem.
Hemosiderin is a hemoglobin derived pigment, it is golden yellow- brown granular intracellular
pigment formed of aggregate of ferritin.
Hemosiderosis: (Localized)
It is accumulation of hemosiderin, primarily within tissue macrophages
without associated tissue or organ damage.
Hemochromatosis: (Generalized Hemosiderosis)
It is more extensive accumulation of hemosiderin often within parenchymal
cells (liver) with associated tissue damage, scarring and organ dysfunction. It may
be hereditary (primary) means the body absorbs too much iron or (secondary) means receiving
too much iron from blood transfusion.Grossly: Organs enlarged, brown & hard.
Liver: cirrhosis.
Heart: arrythmia
Pancreas: diabetes
Skin: bronzed skin due to increase melanin and iron.
Microscopically: Fe in macrophages of liver, spleen & bone
marrow then other organs. iron is taken by macrophages then
taken by parenchymal cells lead to necrosis of these cells.Lipofuscin (Lipochrome)
➢ It is an endogenous, insoluble pigment of complex lipid and protein
structure. It is brownish-yellow granules on both sides of the nucleus.
It is a wear and tear pigment formed by the action of free radicals
on cell membrane lipids.
➢ It commonly accumulates in elderly patients, in whom the pigment is
found most often within hepatocytes and myocardial cells. The
combination of lipofuscin accumulation and atrophy of organs is called
(brown atrophy).Extra cellular deposits
Amyloidosis
Amyloidosis
❑ Deposition of abnormal extracellular fibrillar protein (amyloid) in many
tissues.
❑ Grossly: it is waxy translucent. In Hx & E-stained sections it appears as
homogenous structureless red material (like hyaline degeneration)
❑ Gross amyloid stain
It appears Brown with iodine stain.
It turns blue after adding sulphoric acid to iodine.
❑ In routine Hx and E stained sections it has an amorphous eosinophilic
appearance (stained pink).
❑ Amyloid is stained
red by Congo Red giving an apple-green
birefringence when viewed under polarized light.Clinical patterns of
Amyloidosis
➢ The disease may be systemic or limited (localized) to a single organ.
➢ In systemic amyloidosis, the deposition of amyloid may occur as a primary disease
(e.g. multiple myeloma) or in a secondary form in the course of other disease (
chronic inflammation as Rheumatoid Arthritis).
➢ The nature of the amyloid material: 90% fibril protein which either Amyloid light chain
(AL) or Amyloid associated (AA) in addition to 10% P component.
➢ AL (amyloid light chain): derived from plasma cells. It is usually associated with B
cell neoplasm and multiple myeloma.
➢ AA (amyloid associated): derived from serum amyloid associated protein (SAA) that
increase with chronic inflammatory destructive diseases.Renal amyloidosis
The most common and the most serious form of amyloidosis. kidney is involved
in systemic amyloidosis and so the amyloid is of the AA type.
Grossly: the kidney is slightly enlarged, firm, pale and waxy.
M/E : Amyloid is deposited in glomerular capillary walls and mesangium,
interstitial blood vessels and near the basement membrane of tubules.
The patient usually present with proteinuria, nephrotic syndrome and at last renal
failure.Liver amyloidosis
Part of systemic amyloidosis, amyloid is deposited causing pressure atrophy of
hepatocytes in advanced cases.
Grossly: the liver may be hugely enlarged firm, pale grey waxy
Clinically: there is hepatomegaly
M/E: Amyloid starts to deposit in the wall of sinusoids, central vein and hepatic
arterioles leads to hypoxia and necrosis and the liver plates replaced by
amyloid material (homogenous pink material) leads to chronic liver failure.Amyloid spleen
 The amyloid material is deposited either in central
arterioles of white pulp (nodular pattern or sago spleen)
 Or in the red pulp (map like)(diffuse) compressing the
lymphoid follicles.
 Or it may be mixed both patternsCardiac amyloidosis
 May be part of systemic amyloidosis with AL type amyloid.
 Grossly: The heart is enlarged, with pale, grey-pink subendocardial
deposits.
 M/E: amyloid is deposited between cardiac muscle fibers causing their
atrophy.
 May interfere with the conducting system (arrhythmia). The case ends with
cardiomyopathy and heart failure.Amyloidosis of GIT
 Tongue: Macroglossia.
 Gingiva : thickened.
 Mucosa of the stomach: Thickened amyloid deposition in mucosal
blood vessels, atrophy of epithelial cells, malabsorption, diarrhea.
 Rectal biopsy is an easy way to assess systemic amyloidosis.Pathologic Calcification
Definition:
It is deposition of calcium salts in sites other than bone
and teeth.
Grossly:
As chalk, dull opaque white with fine granular surface &
hard in consistency.
Microscopically:
Dark blue in Hx & E-stained sections.Types
➢ Dystrophic calcification
It is the commonest type. Serum calcium level is normal.
Examples: Occurs in degenerated tissue, old scar, wall of chronic
abscess, fibrosed valve and atheroma.
In Meningioma: called Psammoma bodies.
On top of necrotic tissue: as fat necrosis.
➢ Metastatic calcification
- Occurs in viable tissue. Serum calcium level is high
- Caused by hypercalcemia (increased intake of ca. or hypervitaminosis
D)
➢ Stone formationGout
With increased serum level in blood, uric acid appears in urine & deposited in tissue as Na urates (urate crystals).
Morphology Joints: recurrent acute attacks of arthritis. It affects metatarsophalangeal joint of big toe which become red, hot & swollen (inflammatory arthritis). Kidney: 1. Urate stones 2. Interstitial inflammation , fibrosis & chronic renal failure. 3.Damage to distal tubule and polyuria.