Patterns of Tissue Necrosis

Slide 1 · Patterns of Tissue Necrosis

Six morphologic patterns — causes, gross findings, histology, and clinical interpretation

Preserved tissue

Tissue digestion

Distinct gross findings

Etiologic clues

Dr Abu Suraih Sakhri

MBBS, MD (Pathology)

www.abusuraihsakhri.com

Slide 2 · Learning outcomes

Name and distinguish six morphologic patterns of tissue necrosis.

Predict dominant necrotic appearance from the mechanism and organ involved.

Recognize tissue architecture, nuclear loss, inflammatory debris, and mineral deposition.

Link kidney infarction, cerebral infarction, tuberculosis, pancreatitis, and vascular injury to their typical patterns.

Avoid interpreting a descriptive necrosis pattern as an etiologic diagnosis in isolation.

Slide 3 · Tissue necrosis is a collective process

A tissue becomes necrotic when large numbers of its cells die.

A myocardial infarct is a tissue-level consequence of many myocardial cell deaths.

Individual-cell changes are interpreted within tissue architecture and inflammatory response.

Gross and microscopic patterns offer clues to causation, not definitive proof of an etiology.

Slide 4 · Six recognized descriptive patterns

Coagulative

Preserved tissue framework

Liquefactive

Enzymatic dissolution

Gangrenous

Clinical limb designation

Caseous

Granular necrosis in granuloma

Fat

Lipolysis and calcium soaps

Fibrinoid

Eosinophilic vascular-wall injury

Slide 5 · What determines the dominant appearance?

Protein denaturation

Preservation of cell outlines and tissue framework despite cell death.

Enzymatic digestion

Proteolysis of dead cells and dissolution of tissue architecture.

Site and insult

CNS ischemia, infection, pancreatic enzymes, and vascular immune injury favor different appearances.

Evolution over time

Inflammation, phagocytosis, and calcification modify the initial lesion.

Slide 6 · The central morphologic opposition

Protein / enzyme denaturation

Architecture persists

COAGULATIVE

Predominant enzymatic digestion

Framework dissolves

LIQUEFACTIVE

These are dominant tissue-level morphologies, not mutually exclusive molecular pathways.

Slide 7 · Necrotic cytoplasm on H&E

Increased eosinophilia

Loss of basophilic RNA and accumulation of denatured proteins increase affinity for eosin.

Homogeneous / glassy quality

Loss of intracellular glycogen and structural changes reduce normal granular detail.

Moth-eaten vacuolation

Digestive enzymes destroy organelles and create a vacuolated cytoplasm.

Myelin figures

Whorled phospholipid debris may be phagocytosed, degraded, or associated with calcium deposition.

Slide 8 · Nuclear changes in necrotic cells

Intact nucleus

Distinct nuclear chromatin

Pyknosis

Small, hyperchromatic nucleus

Karyorrhexis

Nuclear fragmentation

Karyolysis

Progressive nuclear fading

Schematic nuclear appearances; All three nuclear endpoints need not be present simultaneously.

Slide 9 · Cell outlines versus tissue dissolution

Viable tissue

Coagulative necrosis

Liquefactive necrosis

Schematic H&E-like fields: Not a photomicrograph; Tissue architecture is illustrated conceptually.

Slide 10 · At the microscope: A systematic approach

Inspect architecture

Preserved or dissolved?

Identify debris

Eosinophilic / granular / fat

Locate inflammation

Neutrophils / granuloma

Check compartment

Parenchyma, fat, vessel

Combine morphology with site, clinical setting, and relevant organism or vascular studies.

Slide 11 · An organ distribution is often diagnostic context

Setting

Dominant pattern

Reason to consider it

Solid-organ ischemic infarct

Coagulative

Protein denaturation; Tissue preserved

CNS infarct

Liquefactive

Digestion and softening

Suppurative infection

Liquefactive

Leukocyte-associated digestion

Tuberculous focus

Caseous

Necrotizing granulomatous process

Acute pancreatitis with fat injury

Fat

Lipase action and calcium soaps

Slide 12 · Molecular cause and gross label are different

Biologic events

Descriptive labels

Loss of cell viability and membrane function.

Enzyme activity and protein damage.

Leukocyte recruitment and clearance.

Firm infarct; Soft suppurative cavity.

Cheeselike focus; Chalky fat deposits.

Necrotic limb; Bright pink vessel wall.

Slide 13 · Coagulative necrosis: Definition

Dead cells persist with their basic tissue architecture recognizable.

A firm gross texture is characteristic.

Cellular outlines can remain visible for at least several days.

Ultimately leukocytes and lysosomal enzymes remove the dead material.

Slide 14 · Why coagulative architecture persists

Severe injury

Often ischemia

Protein denaturation

Structural proteins and enzymes

Proteolysis impeded

Dead cells resist immediate dissolution

Ghost outlines remain

Architecture temporarily retained

Slide 15 · Kidney infarct: Conceptual gross map

Schematic gross section — not a specimen photograph

Pale wedge-shaped infarct

Viable tissue retains perfusion

Ischemia in many solid organs → coagulative necrosis

Slide 16 · Coagulative necrosis at tissue scale

Viable parenchyma

Necrotic ghost outlines

Preserved overall framework

Schematic H&E-like fields: Not a photomicrograph; Tissue architecture is illustrated conceptually.

Slide 17 · Histologic clues to coagulative injury

Tubules or cardiac fibers can remain anatomically recognizable despite cell death.

Cytoplasm becomes more intensely eosinophilic.

Nuclei are lost or show necrotic alterations.

The necrotic territory can recruit an inflammatory infiltrate at its boundary.

A section at one time point cannot establish the exact onset of ischemia.

Slide 18 · Ischemia usually produces coagulative necrosis

Vessel obstruction typically produces coagulative necrosis in solid organs other than the brain.

Localized ischemic tissue necrosis is termed an infarct.

The anatomic distribution and perfusion territory support vascular causation.

The CNS is the principal textbook exception described in this section.

Slide 19 · Coagulative morphology evolves during clearance

Vascular occlusion

Ischemic cell death

Protein denaturation

Framework persists

Leukocyte entry

Enzymatic digestion

Phagocytosis

Dead tissue removed

The sequence is schematic; Exact timing varies with organ, reperfusion, and the host response.

Slide 20 · Firm texture: What the gross appearance tells us

Gross impression

Microscopic confirmation

Firm tissue with preserved structural continuity.

In an infarct, a localized area may appear pale.

Boundaries may become more apparent with inflammatory response.

Cell outlines remain discernible.

Nuclei fade, fragment, or disappear.

Inflammatory cells clear dying tissue over time.

Slide 21 · A key distinction: Infarct is not synonymous with liquefaction

Term

What it denotes

What it does NOT establish

Infarct

Localized ischemic necrosis

A single universal necrosis pattern

Coagulative

Tissue outline preservation

Specific organ or vascular lesion alone

Liquefactive

Dead-tissue digestion

Necessarily an infectious source

Slide 22 · Case: Renal arterial obstruction

A wedge-shaped pale lesion is found in the kidney supplied by an occluded arterial branch. Histology shows intact tubular outlines, markedly eosinophilic cytoplasm, and fading nuclei.

Which pattern best fits the reported architecture?

Coagulative necrosis.

Liquefactive necrosis.

Slide 23 · Renal infarct: Interpretation

Coagulative necrosis is the expected renal infarct pattern.

The decisive clue is preservation of tubular architecture despite dead cells.

The wedge-shaped vascular distribution supports an ischemic infarct.

The lesion is not defined solely by the presence of eosinophilic cytoplasm.

Slide 24 · Liquefactive necrosis: Definition

Enzymatic digestion converts dead tissue into a viscous liquid mass.

Cell and tissue outlines are lost.

The mechanism contrasts with persistence of architecture in coagulative necrosis.

Typical settings are suppurative infections and CNS ischemic injury.

Slide 25 · How digestion predominates

Lethal injury

Microbial or hypoxic

Hydrolytic enzyme activity

Cellular / leukocyte enzymes

Tissue dissolution

Architecture erased

Liquid debris

Soft / viscous necrotic mass

Slide 26 · Suppurative infection: A focused mechanism

Bacterial focus

Sometimes fungal

Leukocyte recruitment

Especially neutrophils

Proteolytic enzymes

Released locally

Pus formation

Creamy yellow debris

Slide 27 · An abscess is an example of liquefaction

Schematic infectious abscess — not clinical microscopy

Neutrophil-rich debris / pus

Peripheral inflamed tissue

Bacterial (and some fungal) infections recruit leukocytes and degradative enzymes.

Slide 28 · Why pus often appears yellow

Leukocytes

Large numbers of inflammatory cells and their breakdown products contribute to creamy yellow material.

Digested tissue

Cellular remnants lose original tissue organization.

Variable microbial burden

The finding is associated with infection but is not an organism identification method.

Diagnostic consequence

Microbiology and site-specific evaluation determine the cause rather than color alone.

Slide 29 · Liquefaction is not synonymous with infection

Hypoxic cell death in the CNS commonly becomes liquefactive, without requiring microbes.

The reason for the CNS preference as not fully understood.

The injured CNS region can soften as tissue undergoes digestion.

Clinical correlation and imaging distinguish ischemia from infection.

Slide 30 · Cerebral infarct: Conceptual progression

Schematic CNS infarct evolution — not radiology or gross pathology

Digested CNS tissue

Softening → possible cavity formation during clearance

Surrounding viable tissue

Slide 31 · Same insult, different organ morphologies

Organ / setting

Typical necrosis pattern

Interpretive emphasis

Kidney, blocked artery

Coagulative

Tubules retain ghost outlines

Heart, blocked artery

Coagulative

Myocyte outlines persist initially

Brain, ischemic injury

Liquefactive

Dissolution / softening of tissue

Bacterial abscess

Liquefactive

Digestive enzymes and pus

Slide 32 · Microscopy: Dissolved versus preserved framework

Coagulative reference

Digestive destruction

Leukocyte-rich debris

Schematic H&E-like fields: Not a photomicrograph; Tissue architecture is illustrated conceptually.

Slide 33 · CNS infarct versus abscess

Ischemic CNS necrosis

Suppurative necrosis

Hypoxic death in central nervous system.

Liquefaction can follow without infection.

Organ context and vascular distribution matter.

Bacterial and occasional fungal foci.

Leukocytes release digestive enzymes.

Pus may accumulate in the lesion.

Slide 34 · Case: Brain tissue softening

A patient develops an ischemic cerebral infarct. At pathologic examination, the affected area is softened, with dissolution of the dead cerebral tissue.

What pattern is expected in the central nervous system?

Liquefactive necrosis.

Coagulative necrosis as in a renal infarct.

Slide 35 · Cerebral infarct: Interpretation

Liquefactive necrosis is typical of ischemic CNS tissue death.

A necrotic cerebral focus commonly loses tissue architecture by digestion.

The liquefactive appearance does not itself mean that bacteria are present.

Robbins explicitly identifies the CNS as an exception to the usual ischemic coagulative pattern.

Slide 36 · Gangrenous necrosis: A clinical label

Gangrene is not a unique microscopic form of cell death.

It usually describes ischemic necrosis affecting a limb or a similar anatomical part.

Underlying injury often shows coagulative necrosis across several tissue planes.

Superinfection can add prominent liquefaction: Wet gangrene.

Slide 37 · The anatomy behind the term

Clinical designation, not a distinct microscopic mechanism

Dry gangrene

Loss of blood supply

Wet gangrene

Ischemic death + bacterial infection

Schematic distal limb segment; No patient photograph.

Slide 38 · Dry gangrene: Ischemia predominates

Blood supply lost

Severe distal ischemia

Multiple tissues die

Limb segment

Coagulative pattern

Architecture relatively retained

Clinical dry gangrene

Term reflects limb context

Slide 39 · Wet gangrene: Infection changes the picture

Necrotic limb

Ischemic substratum

Bacterial superinfection

Secondary process

Bacterial + leukocyte enzymes

More proteolysis

Increased liquefaction

Wet gangrene

Slide 40 · Dry versus wet gangrene

Feature

Dry gangrene

Wet gangrene

Principal setting

Severe ischemic tissue death

Ischemia with superimposed infection

Dominant necrotic process

Usually coagulative

Greater liquefactive component

Tissue context

Often distal limb / multiple tissue planes

Infected necrotic limb / region

Key interpretation

Perfusion failure

Perfusion failure plus infection

Slide 41 · Gangrene is not a histologic diagnosis by itself

What the term conveys

What needs separate assessment

A clinically recognized devitalized region.

Often an ischemic limb segment.

Potentially includes several tissue compartments.

Nature and extent of vascular compromise.

Evidence of infection or suppuration.

Tissue viability at the margins.

Slide 42 · Why the “wet” qualifier matters

Second mechanism

Bacterial and recruited leukocyte enzymes increase digestion beyond the ischemic lesion.

Multiple compartments

The process is not limited to one microscopic cell type.

Clinical consequence

The adjective highlights possible superinfection rather than a new fundamental death pathway.

Interpretive limit

Neither gross discoloration nor the word gangrene identifies the specific infectious organism.

Slide 43 · Case: Necrotic lower leg with infection

An ischemic lower leg has already become necrotic. A bacterial infection supervenes and the lesion develops pronounced tissue liquefaction.

What makes the process “wet gangrene”?

Additional bacterial and leukocytic enzymatic digestion.

Exclusive mitochondrial apoptosis without inflammation.

Slide 44 · Gangrene case: Interpretation

Wet gangrene adds infection-associated liquefaction to ischemic necrosis.

The ischemic substratum commonly displays a coagulative component.

The term describes an anatomic and clinical scenario, not a seventh pathway of cellular death.

The possibility of infection must be assessed independently of appearance.

Slide 45 · Caseous necrosis: Distinctive appearance

Caseous necrosis produces friable, white, cheeselike necrotic material.

Classically associated with tuberculous infection.

Microscopy shows amorphous granular debris with loss of recognizable tissue structures.

The necrosis may be surrounded by epithelioid histiocytes in a granuloma.

Slide 46 · Gross caseation: Descriptive clues

White to yellow-white

The pale color is a gross descriptive cue rather than a specific chemical test.

Friable / crumbly

The surface differs from the firm architecture of coagulative necrosis.

Loss of recognizable tissue

Destroyed cells merge into a granular necrotic mass.

Context

A necrotizing granuloma supports an infectious differential, especially tuberculosis.

Slide 47 · A caseating granuloma: Architecture

Schematic caseating granuloma — not a histologic section

Central caseous debris

Epithelioid histiocytes / lymphocytes

Slide 48 · Caseous necrosis under the microscope

The center is structureless and composed of fragmented or lysed cells.

Amorphous granular eosinophilic necrotic debris replaces recognizable structures.

A surrounding zone of epithelioid histiocytes indicates granulomatous inflammation.

Ancillary organism testing may be required to determine the etiology.

Slide 49 · Why a granuloma matters

Persistent local insult

Classically mycobacterial

Macrophage accumulation

Epithelioid differentiation

Granuloma architecture

Organized inflammatory focus

Central caseation

Structureless necrotic debris

Slide 50 · Caseation is a clue, not microbiologic proof

Morphology can support

Morphology alone cannot confirm

Necrotizing granulomatous inflammation.

A tuberculosis-centered differential in an appropriate setting.

Selection of microbiologic / special-stain studies.

Species of causative organism.

Active infection status and viable organisms.

A single etiologic diagnosis in every case.

Slide 51 · Caseous versus coagulative necrosis

Feature

Caseous

Coagulative

Gross

White, friable, cheeselike

Firm, organized tissue

Microscopic architecture

Amorphous granular debris

Ghost cellular outlines persist

Typical context

Tuberculous granuloma

Solid-organ ischemia

Inflammatory organization

Epithelioid granulomatous rim

Leukocyte clearance of dead tissue

Slide 52 · Case: Lung lesion with granulomatous rim

A pulmonary focus contains soft, friable white necrotic material. Histology shows amorphous granular debris circumscribed by epithelioid histiocytes.

What pattern is present, and what association must be considered?

Caseous necrosis; Tuberculosis is an important possibility.

Coagulative necrosis; Isolated arterial occlusion is obligatory.

Slide 53 · Caseating lung lesion: Interpretation

Caseous necrosis in a granulomatous inflammatory setting.

Friable gross debris and amorphous microscopic necrosis support the pattern.

Tuberculosis is a classic association.

Additional studies establish the organism; This morphology is not a standalone microbiologic diagnosis.

Slide 54 · Fat necrosis: Destruction of adipose tissue

Activated pancreatic lipases can destroy fat around the pancreas and in the peritoneal cavity.

Damaged pancreatic acinar cells permit enzyme leakage.

Triglycerides are hydrolyzed to fatty acids.

Released fatty acids bind calcium to produce grossly visible chalky deposits.

Slide 55 · Pancreatic enzyme escape: The sequence

Acinar injury

Pancreatic enzyme escape

Fat cell destruction

Membranes damaged

Triglycerides hydrolyzed

Lipase activity

Fatty acids + Ca²⁺

Saponification

Slide 56 · The chemistry of fat saponification

Adipocyte damage

Activated pancreatic lipases

Triglyceride hydrolysis

Free fatty acids released

Fatty acids + calcium

Chalky-white calcium soaps

Hydrolyzed lipid

Calcified soap deposits

Schematic pathway: Calcium deposition occurs in damaged fat, not in simple fatty change.

Slide 57 · Fat necrosis: Key gross characteristic

Chalky-white deposits

Grossly evident calcium soaps form in areas of damaged peripancreatic / peritoneal fat.

Localized fat destruction

Lipase injury involves adipose structures beyond the pancreatic parenchyma.

Inflammation

Local reactions accompany necrotic adipocyte breakdown and calcium deposition.

Clinical context

In severe acute pancreatitis, this morphology provides a conspicuous clue to enzymatic fat damage.

Slide 58 · Fat necrosis: Histologic pattern

Schematic H&E fat necrosis — not a photomicrograph

Ghost outlines of adipocytes

Basophilic calcium deposits with inflammation

Slide 59 · The histologic triad to recognize

Finding

Interpretation

Shadowy adipocyte outlines

Necrotic fat cells remain recognizable as empty ghosts

Basophilic calcium deposits

Local calcium soap deposition after fatty-acid formation

Inflammatory reaction

Host response to fat-cell destruction

Slide 60 · Fat necrosis and dystrophic calcification

Dead adipocytes

Necrotic fat

Lipid breakdown

Free fatty acids

Calcium binding

Soap formation

Visible deposits

Chalky / basophilic material

Slide 61 · Fat necrosis ≠ fatty change

Fat necrosis

Fatty change (steatosis)

Destruction of fat cells.

Release of fatty acids and calcium soap formation.

Inflammatory reaction and necrotic adipocyte outlines.

Triglyceride accumulation within viable parenchymal cells.

Classically described in liver injury contexts.

Does not by itself imply fat-cell death or saponification.

Slide 62 · Enzymatic fat necrosis is a tissue clue

Recognize that the damaged substrate is fat, not just pancreatic acinar tissue.

Connect fat-cell membranes, triglycerides, released fatty acids, and calcium soaps.

Interpret basophilic calcific deposits with adipocyte ghost outlines.

Avoid confusing small lipid vacuoles in viable hepatocytes with dead adipose tissue.

Slide 63 · Case: Acute pancreatitis and mesenteric chalk

During surgery for severe acute pancreatitis, multiple chalky-white foci are observed in peritoneal fat. Histology shows outlines of dead adipocytes and basophilic deposits.

Which pathogenesis best accounts for the finding?

Pancreatic lipase-mediated fat injury with calcium saponification.

A purely reversible intracellular triglyceride accumulation.

Slide 64 · Pancreatic fat necrosis: Interpretation

Enzymatic fat necrosis with calcium soap formation.

Activated pancreatic lipases hydrolyze adipocyte triglycerides.

Free fatty acids combine with calcium to create chalky deposits.

Adipocyte shadows plus basophilic calcium are characteristic histologic clues.

Slide 65 · Fibrinoid necrosis: Vascular-wall damage

Fibrinoid necrosis describes a striking bright-pink, amorphous lesion of vessel walls.

Vascular immune reactions as a typical setting.

Antigen–antibody complexes may accumulate in arterial walls.

Leaked plasma proteins contribute to fibrin-like eosinophilic material.

Slide 66 · Immune-mediated vascular injury

Vascular immune reaction

Antigen–antibody complexes

Vessel-wall deposition

Local tissue injury

Plasma-protein leakage

Permeability disturbance

Fibrinoid appearance

Bright pink amorphous wall

Slide 67 · Where to look: Vessel wall, not parenchymal core

Schematic vessel-wall injury — not a histologic micrograph

Bright pink amorphous vascular-wall material

Lumen with altered wall architecture

Actual fibrinoid necrosis is interpreted with vessel injury and clinical context.

Slide 68 · Fibrinoid necrosis at H&E

Examine injured vessels for intensely eosinophilic material involving the wall.

The material is amorphous, with a fibrin-like microscopic appearance.

Immune deposits and leaked plasma proteins contribute to this appearance.

The pattern belongs to vascular damage and requires relevant clinical and histologic context.

Slide 69 · Why “fibrinoid” is a morphologic term

Descriptive resemblance

“Fibrinoid” refers to a bright pink, fibrin-like H&E appearance.

Not a molecular assay

The term does not by itself demonstrate pure fibrin as the only constituent.

Anatomical location

Interpretation depends on the material being in damaged vessel walls.

Causal possibilities

Immune-complex reactions as a common context.

Slide 70 · Fibrinoid versus other eosinophilic necrosis

Pattern

Dominant location

Recognition clue

Fibrinoid

Vessel wall

Amorphous bright pink, fibrin-like material

Coagulative

Parenchymal infarct

Preserved dead tissue framework

Caseous

Necrotizing granuloma

Granular acellular center + epithelioid rim

Slide 71 · Case: Immune injury in an artery

A small artery affected by an immune-mediated disorder has a circumferential, bright-pink amorphous lesion of its wall, with local inflammation.

Which descriptive type of necrosis is most appropriate?

Fibrinoid necrosis.

Fat necrosis with pancreatic saponification.

Slide 72 · Fibrinoid vascular lesion: Interpretation

Fibrinoid necrosis describes the eosinophilic vascular-wall damage.

The crucial compartment is the wall of the affected artery.

Immune-complex deposition and plasma-protein escape are common associated processes.

Etiologic diagnosis still requires broader vascular and clinical assessment.

Slide 73 · All six patterns: Morphology and setting

Pattern

Morphologic hallmark

Classic example

Coagulative

Firm; Architecture retained

Renal / myocardial infarct

Liquefactive

Digested; Viscous debris

Cerebral infarct or abscess

Gangrenous

Necrotic limb; ± infection

Ischemic lower limb

Caseous

Friable debris in granuloma

Tuberculosis

Fat

Adipocyte ghosts; Calcium soaps

Acute pancreatitis

Fibrinoid

Pink amorphous vessel wall

Immune vascular injury

Slide 74 · Pattern recognition: Organ, then architecture

Which tissue?

Solid organ / brain / fat / vessel

Preserved framework?

Yes → coagulative

Digested or special material?

Pus, granuloma, soaps

Clinical context

Validate etiologic inference

Slide 75 · A pattern is not proof of one cause

Coagulative → think ischemia

Check vascular distribution and organ findings; Architecture alone does not establish a particular artery.

Liquefactive → infection OR CNS ischemia

Do not equate liquefaction automatically with a bacterial process.

Caseous → consider tuberculosis

The granulomatous necrosis guides testing but does not independently identify the organism.

Fibrinoid → assess vascular injury

Evaluate immune and other vessel-wall insults in context.

Slide 76 · What happens to necrotic debris?

Necrotic cells persist

Dead tissue and debris

Enzymatic digestion

Resident / recruited enzymes

Phagocytic clearance

Leukocytes ingest remnants

Possible mineralization

If debris remains

Slide 77 · Dystrophic calcification: An endpoint, not a type

Early injury signature

If necrotic remnants persist

Coagulative, liquefactive, and other patterns describe dominant morphology.

Their causes vary with organ and insult.

Debris is frequently cleared by host cells.

Calcium and other minerals may deposit.

Deposits can follow multiple forms of dead-tissue injury.

Fat saponification is a specific calcium soap mechanism.

Slide 78 · Knowledge check: Tissue preservation

An infarcted kidney retains tubule outlines despite nuclear loss. The pattern is:

(A) Coagulative necrosis.

(B) Liquefactive necrosis.

(C) Caseous necrosis.

(D) Fibrinoid necrosis.

Slide 79 · Knowledge check: Tissue preservation

Coagulative necrosis preserves outlines of dead renal tissue.

The architecture persists because protein and enzyme denaturation impedes rapid breakdown.

Solid-organ ischemia is the classic cause.

The ischemic area may subsequently be cleared by leukocytes.

Slide 80 · Knowledge check: Match the mechanism

Which finding most strongly supports pancreatic enzymatic fat necrosis?

(A) Calcium soaps and ghost adipocytes.

(B) Preserved renal tubules with vanished nuclei.

(C) Bright pink immune-damaged vessel walls.

(D) Caseating granuloma with central granular debris.

Slide 81 · Knowledge check: Fat injury

Lipase-mediated hydrolysis and calcium soaps are characteristic.

Fat-cell destruction releases triglycerides for enzymatic hydrolysis.

Fatty acids bind calcium, producing chalky deposits.

Histology shows necrotic adipocyte outlines and basophilic calcium.

Slide 82 · Summary: Six patterns, three interpretive rules

Architecture retained → think coagulative; Tissue liquefied → think enzymatic digestion.

CNS ischemia and suppurative infection are different causes of liquefactive necrosis.

Gangrene is a clinical label; Wet gangrene adds infection-associated liquefaction.

Caseous granulomas, chalky fat necrosis, and fibrinoid vessel injury have distinctive tissue compartments.

Use morphology to generate and prioritize diagnoses—not to replace etiologic testing.

Slide 83 · Textbook source and visual provenance

Robbins, Cotran & Kumar: Pathologic Basis of Disease. 11th ed. (2026), Chapter 2, “Patterns of Tissue Necrosis,” pp. 38–40.

Included adjacent cell-level morphologic material (“Morphology,” pp. 38–39).

Six-pattern description, organ examples, and calcium deposition concepts follow the primary Robbins excerpt.

All displayed pathology-like tissue drawings are original, explicitly labeled schematics; they are NOT photomicrographs.

No copyrighted Robbins figure or other externally sourced histologic specimen is reproduced.