Morphologic Patterns of Acute Inflammation

Slide 1 · Morphologic Patterns

of Acute Inflammation

Recognizing exudates, surface lesions, and outcomes

Serous fluid

Fibrin

Pus / abscess

Ulceration

Dr Abu Suraih Sakhri

MBBS, MD (Pathology)

www.abusuraihsakhri.com

Slide 2 · Morphologic recognition: Learning objectives

Identify the shared vascular and cellular hallmarks of acute inflammation.

Distinguish serous, fibrinous, purulent, and ulcerative patterns by their material and architecture.

Explain how severity, cause, and anatomic site shape the appearance.

Link each pattern to a characteristic clinical example and potential outcome.

SEROUS

Fluid-rich

FIBRINOUS

Fibrin deposit

PURULENT

Pus + debris

ULCER

Surface defect

Slide 3 · Acute inflammation has a common morphologic substrate

Dilated small vessels increase blood flow at the injured site.

Plasma-derived fluid accumulates outside vessels.

Leukocytes—often initially neutrophils—collect in affected tissues.

Special patterns add a dominant exudate or a distinctive tissue defect.

Small vessel

Extravascular tissue

Increased permeability → fluid + cells

Slide 4 · Two hallmarks: Vascular dilation and extravasation

Dilation is a change in intravascular caliber and local perfusion.

Extravasation moves fluid and leukocytes into interstitial compartments.

The amount and composition of escaped material influence the appearance.

Site-specific architecture determines where exudate is visible.

Small vessel

Extravascular tissue

Increased permeability → fluid + cells

Slide 5 · The exudate reflects the local vascular response

Increased endothelial permeability allows plasma components to leave the circulation.

Greater permeability can permit large proteins, including fibrinogen, to escape.

Leukocyte accumulation and cell injury may add cellular debris.

Classify the dominant pattern rather than assuming one component is exclusive.

Small vessel

Extravascular tissue

Increased permeability → fluid + cells

Slide 6 · Why identical triggers need not look identical

Intensity of injury influences vascular leakage and tissue destruction.

Nature of the stimulus influences cellular recruitment and local reactions.

Tissue architecture determines whether fluid pools, coats a surface, or forms a cavity.

Host responses and time alter the observed stage of a lesion.

Severity of injury

Amount of leakage / necrosis

Nature of stimulus

Cellular and exudative response

Tissue and location

Visible space, surface or crater

Slide 7 · Four major gross and microscopic patterns

Serous: Predominantly serum-like fluid.

Fibrinous: Deposited fibrin within tissue or on a serosal surface.

Purulent: Pus rich in neutrophils and liquefied cellular debris.

Ulceration: Loss of surface tissue after necrosis and sloughing.

SEROUS

Fluid-rich

FIBRINOUS

Fibrin deposit

PURULENT

Pus + debris

ULCER

Surface defect

Slide 8 · Morphology suggests—but does not prove—etiology

Serous fluid commonly has few leukocytes and no demonstrable microbes.

Pyogenic bacteria are frequent triggers of pus formation.

Fibrin deposition suggests marked vascular leakage plus local coagulation.

An ulcer identifies superficial necrosis, not one specific cause.

Observe material

Fluid → serous

Fibrin → fibrinous

Pus → suppurative

Surface defect → ulcer

Slide 9 · Reading a lesion: Start with the compartment

Is the dominant abnormality in a body cavity, tissue space, or surface?

Is there intact overlying epithelium, surface fibrin, or a true crater?

Are there numerous neutrophils and liquefied necrotic cells?

Look for concurrent features and evolution over time.

Where is the lesion?

What dominates the exudate?

Is there necrosis / tissue loss?

Is repair occurring?

Slide 10 · A practical classification matrix

Pattern

Dominant material

Structural clue

Classical example

Serous

Serum-like fluid; Few leukocytes

Blister or serosal effusion

Burn-related skin blister

Fibrinous

Extracellular fibrin

Eosinophilic threads / surface coagulum

Fibrinous pericarditis

Purulent

Neutrophils + liquefied debris

Pus; Localized if abscess

Pyogenic abscess / appendicitis

Ulcer

Sloughed necrotic surface tissue

Loss of epithelium; Crater

Peptic or lower-leg ulcer

Patterns describe predominant morphology; Mixtures and transitions can occur.

Slide 11 · Serous inflammation: The defining material

Serum-like fluid enters tissue spaces created by cell injury.

Fluid can also accumulate within mesothelium-lined body cavities.

Large numbers of leukocytes are not the dominant component.

Serous does not automatically mean a sterile process has been proven.

Separated epidermal roof

Serous fluid pocket

Dermis

Original schematic · not a specimen

Slide 12 · The fluid-filled space is an anatomic clue

Skin blister: Fluid accumulates within or immediately below injured epidermis.

Pericardial, pleural, and peritoneal spaces may contain a serous effusion.

Histologic emphasis is separation/distension by fluid rather than pus or dense fibrin.

Separated epidermal roof

Serous fluid pocket

Dermis

Original schematic · not a specimen

Slide 13 · How a skin blister develops

A burn or certain viral infections injure the epidermal compartment.

Fluid accumulates inside or beneath the damaged epithelial layer.

The resulting separation creates a clinically visible blister.

The schematic depicts a location of fluid—not a particular viral diagnosis.

Separated epidermal roof

Serous fluid pocket

Dermis

Original schematic · not a specimen

Slide 14 · Serous inflammation in mesothelium-lined cavities

Pleural, pericardial, and peritoneal spaces can collect fluid.

The collected fluid is described as an effusion.

A serosal surface may remain relatively smooth when little fibrin is deposited.

Fluid location alone cannot determine whether an effusion is inflammatory.

Serosal effusion

Visceral / parietal linings

Original schematic · not a specimen

Slide 15 · Two possible origins of an inflammatory effusion

Plasma may escape when local vascular permeability increases.

Irritated mesothelial cells can contribute fluid to the cavity.

Either mechanism may occur in a serosal space.

The term effusion describes location rather than biochemical mechanism.

Serosal effusion

Visceral / parietal linings

Original schematic · not a specimen

Slide 16 · Cellularity in a typical serous response

Serous fluid usually lacks large numbers of leukocytes.

A heavy neutrophilic component would favor a purulent pattern.

Inflammatory lesions can evolve: Mixed or changing patterns may coexist.

Interpret fluid morphology with the involved tissue and clinical setting.

Small vessel

Extravascular tissue

Increased permeability → fluid + cells

Slide 17 · Effusion is not synonymous with inflammation

Inflammatory effusion can reflect vascular permeability or mesothelial irritation.

Heart failure may yield fluid through altered blood outflow.

Low plasma protein levels in kidney or liver disease can also yield fluid.

An effusion therefore requires etiologic interpretation beyond appearance.

Serosal effusion

Visceral / parietal linings

Original schematic · not a specimen

Slide 18 · Serous versus noninflammatory fluid: Reasoning

Ask whether the patient has local injury or serosal inflammation.

Consider circulatory congestion or low plasma oncotic pressure as alternatives.

Do not infer infection simply from the presence of fluid.

Laboratory classification requires measurements not specified in this topic.

Serosal effusion

Visceral / parietal linings

Original schematic · not a specimen

Slide 19 · Serous morphology: What to describe

Location of the fluid relative to epithelial or serosal layers.

Degree of separation/distension of the involved compartment.

Presence or absence of conspicuous neutrophils, fibrin, and necrotic debris.

Whether the surface remains intact or is already ulcerated.

Separated epidermal roof

Serous fluid pocket

Dermis

Original schematic · not a specimen

Slide 20 · Clinical example: Burn-related blister

A raised fluid-filled lesion follows epidermal injury.

The principal material is a collection of serum-like fluid.

The fluid does not, by itself, indicate an abscess.

Morphologic diagnosis: Serous inflammation in a damaged epithelial compartment.

Separated epidermal roof

Serous fluid pocket

Dermis

Original schematic · not a specimen

Slide 21 · Serous pattern: Reversible injury versus progression

If damage is limited and the initiating stimulus ends, fluid can be resorbed.

Macrophages and lymphatic drainage participate in clearing inflammatory material.

Sustained injury may produce a more cellular exudate or tissue destruction.

Interpret an isolated image as one point in an evolving process.

Limited injury

Clearance of debris + fluid

Tissue restoration

Slide 22 · Fibrinous inflammation: More than fluid leakage

Greater permeability permits fibrinogen and other large plasma proteins to escape.

A local procoagulant stimulus promotes fibrin formation.

Deposited fibrin becomes the dominant morphologic material.

Fibrinous exudates are prominent along inflamed serosal surfaces.

Fibrin strands on a serosal surface

Underlying serosal tissue

Original schematic · not a specimen

Slide 23 · From fibrinogen leakage to fibrin deposition

Vascular permeability increases sufficiently for fibrinogen extravasation.

Local coagulation turns fibrinogen into insoluble fibrin.

Threads of fibrin coat a surface or accumulate in extravascular tissue.

This is a causal sequence, not a quantitative permeability threshold.

Fibrin strands on a serosal surface

Underlying serosal tissue

Original schematic · not a specimen

Slide 24 · Anatomic predilection of fibrinous exudate

Pericardial and pleural surfaces are important sites.

Meningeal surfaces can also show a fibrinous exudate.

Serosa creates an accessible surface on which fibrin deposits are grossly visible.

Name the involved surface before describing the exudate.

Pericardium

Pleura

Meninges

Slide 25 · Gross fibrinous pericarditis: Surface deposition

Fibrin coats the pericardial surface rather than forming an intraparenchymal abscess.

Exudate may produce an opaque, roughened surface.

Compare the smooth normally apposed layers with fibrin-bearing layers.

Dense deposition may later lead to fibrous thickening.

Fibrin deposition

Pericardial surfaces

Original schematic · not a specimen

Slide 26 · Fibrin on microscopy: Eosinophilic threads

Fibrin often forms an eosinophilic meshwork on H&E sections.

It may alternatively appear as an amorphous eosinophilic coagulum.

Identify the serosal tissue beneath the deposited material.

The diagram is schematic; Actual photomicrograph interpretation requires a specimen.

Extracellular fibrin: A dense eosinophilic network

Serosal connective tissue

Original schematic · not a specimen

Slide 27 · Why fibrin may appear amorphous

Fibrin can aggregate into a relatively homogeneous-appearing surface layer.

Its thread-like quality varies with section orientation and density.

Both meshwork and amorphous coagulum are recognized textbook patterns.

The key observation remains extracellular fibrin deposition.

Extracellular fibrin: A dense eosinophilic network

Serosal connective tissue

Original schematic · not a specimen

Slide 28 · Fibrinous exudate can be removed

Fibrinolysis may dissolve deposited fibrin.

Macrophages can clear the resulting material.

A successfully cleared exudate need not leave a permanent scar.

Complete removal is more likely when persistent injury is controlled.

Deposited fibrin

Fibrinolysis + macrophages

Fibrovascular ingrowth

Clearance

Organization → scar

Slide 29 · Failure of fibrin clearance leads to organization

Persistent fibrin provides a substrate for tissue ingrowth.

Fibroblasts and new blood vessels invade the exudate.

Connective tissue replaces the original fibrin deposit.

The name for this replacement process is organization.

Deposited fibrin

Fibrinolysis + macrophages

Fibrovascular ingrowth

Clearance

Organization → scar

Slide 30 · Organized pericardial exudate changes anatomy

Fibrous tissue may thicken pericardial and epicardial surfaces.

Extensive organization can obliterate the pericardial space.

Loss of the normal serosal plane is a structural consequence of persistent exudate.

Do not infer functional severity solely from a schematic.

Fibrous bridging / organization

Pericardial surfaces

Original schematic · not a specimen

Slide 31 · Clearance or fibrosis: The two trajectories of fibrin

Removal: Fibrinolysis plus macrophage clearance.

Organization: Fibroblast and vascular ingrowth.

The balance depends on persistence and clearance of the injury/exudate.

Organization is not identical to ongoing fibrin deposition.

Deposited fibrin

Fibrinolysis + macrophages

Fibrovascular ingrowth

Clearance

Organization → scar

Slide 32 · Distinguish fibrinous from serous inflammation

Serous: Conspicuous fluid with relatively sparse cells.

Fibrinous: Conspicuous eosinophilic strands or surface coagulum.

Fibrin requires large protein leakage plus a coagulation-promoting environment.

Mixed serofibrinous appearances may occur in real tissue.

Serous fluid

Fibrin threads

Original schematic · not a specimen

Slide 33 · Interpretation exercise: An opaque pericardial coat

Observed: A roughened serosal surface with an adherent fibrin-rich exudate.

Pattern: Fibrinous inflammation.

Outcome to watch: Clearance versus fibrous organization.

Pattern recognition cannot establish a unique etiology.

Fibrin deposition

Pericardial surfaces

Original schematic · not a specimen

Slide 34 · Purulent inflammation is defined by pus

Pus is an exudate containing neutrophils, liquefied cellular debris, and edema fluid.

Localized tissue destruction gives the fluid a turbid or creamy appearance.

The pattern is also termed suppurative inflammation.

Its common cause is infection by pyogenic bacteria.

Neutrophils + liquefied necrotic material

Original schematic · not a specimen

Slide 35 · The constituents of pus have different origins

Neutrophils arrive through inflammatory leukocyte recruitment.

Necrotic tissue cells and leukocytes contribute cellular debris.

Edema fluid supplies the liquid phase.

Microbial organisms may be present depending on the cause and sampling.

Neutrophils + liquefied necrotic material

Original schematic · not a specimen

Slide 36 · Why pyogenic infections produce suppuration

Certain bacteria provoke marked neutrophilic responses.

Tissue digestion and neutrophil breakdown contribute to liquefactive necrosis.

Staphylococci are a textbook example of pyogenic bacteria.

Purulent morphology strongly suggests, but does not independently prove, a bacterial cause.

Pyogenic stimulus

Neutrophils recruited

Liquefactive necrosis

Pus formation

Slide 37 · Neutrophil-rich inflammation versus true pus

Acute inflammation can recruit neutrophils before pus develops.

Pus additionally contains liquefied tissue and leukocyte debris.

A dense cellular infiltrate alone is not identical to an abscess cavity.

Architecture and necrosis must be assessed together.

Neutrophils in tissue

Liquefactive necrosis

Original schematic · not a specimen

Slide 38 · Acute appendicitis as a suppurative example

Acute appendicitis as a common example of suppurative inflammation.

The dominant acute cellular population is neutrophilic.

Use tissue context rather than gross color alone to classify the response.

Appendicitis is an example—not a morphologic definition of all purulence.

Neutrophils + liquefied necrotic material

Original schematic · not a specimen

Slide 39 · Abscess: Pus localized in a confined focus

An abscess is a circumscribed collection of pus.

It may form in tissue, within an organ, or in a confined space.

Pyogenic bacterial seeding is an important mechanism.

The architecture distinguishes an abscess from diffuse suppuration.

Necrotic center · viable neutrophil rim

Original schematic · not a specimen

Slide 40 · Abscess architecture has recognizable zones

Center: Liquefied necrotic leukocytes and tissue cells.

Inner surrounding zone: More preserved neutrophils.

Outer zone: Dilated vessels and tissue response.

Chronic inflammation and repair may develop beyond the acute focus.

Necrotic center · viable neutrophil rim

Original schematic · not a specimen

Slide 41 · The center of an abscess is liquefied tissue

Tissue architecture is lost within the necrotic center.

Necrotic neutrophils mix with destroyed parenchymal cells.

Fluid-rich debris forms the abscess core.

Distinguish this focus from intact, viable tissue at the periphery.

Necrotic center · viable neutrophil rim

Original schematic · not a specimen

Slide 42 · The abscess rim shows host containment

Neutrophils persist around the central necrotic compartment.

Adjacent small vessels may be markedly dilated.

Outside the rim, proliferating stromal cells and vessels signal repair.

The spatial pattern helps establish lesion age and response.

Necrotic center · viable neutrophil rim

Original schematic · not a specimen

Slide 43 · Evolution: Abscess walling-off and fibrosis

The acute purulent focus may become increasingly circumscribed.

Fibroblastic proliferation can form a more distinct peripheral wall.

Over time, connective tissue may replace the focus.

Persistent infection can prevent timely resolution.

Bacterial seeding

Purulent focus

Walling-off

Fibrous replacement

Slide 44 · Abscess versus diffuse purulent inflammation

Abscess: A localized necrotic fluid collection in a defined compartment.

Diffuse suppuration: Neutrophilic exudate spread through a tissue or surface.

Both may be caused by pyogenic bacteria.

Localization is an anatomic observation, not a separate microbial species.

Confined abscess

Diffuse suppuration

Original schematic · not a specimen

Slide 45 · Do not confuse fibrin with purulent debris

Fibrin: Mainly deposited extracellular protein with thread-like/coagulated texture.

Pus: Mainly neutrophils, necrotic cells, and edema fluid.

Fibrin and neutrophils can coexist in mixed inflammatory exudates.

Describe the dominant material and the tissue damage.

Extracellular fibrin

Neutrophils + debris

Original schematic · not a specimen

Slide 46 · Clinical scenario: A focal lung collection

Gross finding: A discrete cavity filled with thick inflammatory material.

Histologic concept: Liquefaction centrally and neutrophils around it.

Morphologic designation: Pulmonary abscess.

Morphology establishes a suppurative pattern, not the responsible organism.

Necrotic center · viable neutrophil rim

Original schematic · not a specimen

Slide 47 · Ulcer: A defect created by tissue loss

Ulceration is focal loss or excavation of an organ or tissue surface.

Inflamed necrotic tissue sloughs, leaving a surface defect.

Ulceration therefore requires necrosis at or near a surface.

Its hallmark is tissue absence—not a particular type of exudate.

Surface loss / crater

Inflamed tissue beneath defect

Original schematic · not a specimen

Slide 48 · Surface location is essential for ulceration

A mucosal or cutaneous epithelial boundary is a typical site.

Destruction beneath an intact surface may instead produce an internal focus.

When surface tissue detaches, a visible excavation remains.

The underlying inflammatory response may be acute, chronic, or mixed.

Surface loss / crater

Inflamed tissue beneath defect

Original schematic · not a specimen

Slide 49 · From surface injury to an ulcer crater

Surface epithelium becomes injured and necrotic.

Damaged tissue is shed from the surface.

A depressed crater exposes inflamed underlying tissue.

Sustained injury recruits additional inflammatory cells and repair reactions.

Surface necrosis

Sloughing

Tissue crater

Repair / chronicity

Slide 50 · Common mucosal sites of ulceration

Mouth, stomach, intestines, and genitourinary tract are recognized sites.

Peptic ulcers in the stomach or duodenum are classic examples.

Describe the involved epithelial compartment and defect depth.

The same term “ulcer” does not specify the primary disease.

Mouth / GI mucosa

Genitourinary mucosa

Skin

Slide 51 · Lower-extremity ulcers: Vascular susceptibility

Skin and subcutaneous tissues of the lower extremity are frequent sites.

Vascular insufficiency predisposes tissue to damage and impaired repair.

Diabetes, sickle cell anemia, and peripheral vascular disease.

Risk factors are not interchangeable with a histologic diagnosis.

Reduced tissue perfusion

Peripheral vascular disease

Diabetes-related vulnerability

Sickle cell disease

Slide 52 · Acute ulcer margin: Active tissue injury

Neutrophils accumulate at the margins and surface.

Vascular dilation contributes to hyperemia around the defect.

Necrotic debris may be present in the crater.

Acute inflammation is most prominent in actively injured regions.

Surface loss / crater

Inflamed tissue beneath defect

Original schematic · not a specimen

Slide 53 · Chronic ulcer base: Repair coexists with injury

Fibroblasts proliferate as a repair response.

Collagenous scar develops within the base and edges.

Lymphocytes, macrophages, and plasma cells can accompany chronicity.

Active neutrophils and chronic reparative tissue may occur together.

Surface loss / crater

Repair and fibrosis at base

Original schematic · not a specimen

Slide 54 · Peptic ulcer as an acute–chronic interface

Gastric or duodenal peptic ulceration to demonstrate mixed inflammation.

The crater records surface necrosis and sloughing.

An acutely inflamed region may overlie more chronic fibrosis and cells.

The pattern is an excavation with superimposed inflammatory layers.

Surface loss / crater

Inflamed tissue beneath defect

Original schematic · not a specimen

Slide 55 · Ulceration versus abscess: The discriminant

Ulcer: Surface loss and excavation following necrosis.

Abscess: A localized collection of liquefied necrotic tissue and pus.

An ulcer may develop secondary purulent exudate at its base.

One lesion may display features of both, but their definitions remain distinct.

Surface tissue lost

Pus-filled cavity

Original schematic · not a specimen

Slide 56 · Describe an ulcer with tissue-based language

Identify location: Skin or specific mucosa.

Identify the defect: Surface loss, exposed base, and margins.

Describe inflammatory components: Neutrophils versus mononuclear cells.

Assess the reparative component: Fibroblasts and scar tissue.

Surface loss / crater

Inflamed tissue beneath defect

Original schematic · not a specimen

Slide 57 · Clinical scenario: A chronic duodenal crater

A mucosal defect has acute neutrophilic exudate at its exposed base.

Fibrosis and chronic inflammatory cells occur deeper and at the margins.

The lesion is an ulcer with concurrent acute and chronic inflammation.

The morphological description does not establish its specific upstream cause.

Surface loss / crater

Inflamed tissue beneath defect

Original schematic · not a specimen

Slide 58 · Read four patterns by the dominant observation

Pattern

Dominant material

Structural clue

Classical example

Serous

Serum-like fluid; Few leukocytes

Blister or serosal effusion

Burn-related skin blister

Fibrinous

Extracellular fibrin

Eosinophilic threads / surface coagulum

Fibrinous pericarditis

Purulent

Neutrophils + liquefied debris

Pus; Localized if abscess

Pyogenic abscess / appendicitis

Ulcer

Sloughed necrotic surface tissue

Loss of epithelium; Crater

Peptic or lower-leg ulcer

Patterns describe predominant morphology; Mixtures and transitions can occur.

Slide 59 · A single specimen can show overlapping patterns

Serous fluid may coexist with fibrin deposition.

Fibrin and neutrophilic exudate may coexist on an inflamed surface.

An ulcer base may contain neutrophils, debris, and scar.

Use precise descriptive terms and identify the dominant process.

One specimen

Fluid + fibrin

Fibrin + neutrophils

Ulcer + necrotic debris

Chronic repair + acute cells

Slide 60 · Three major outcomes of acute inflammation

Resolution restores tissue when injury is limited and cells can regenerate.

Fibrosis follows major destruction, impaired regeneration, or unremoved fibrin.

Chronic inflammation may follow persistence of the injurious stimulus.

Clinical and anatomic context helps predict which pathway is likely.

Limited injury → resolution

Major damage → fibrosis

Persistent stimulus → chronicity

Slide 61 · Outcome follows the material that must be cleared

Fluid: Resorption and drainage can restore an undamaged compartment.

Fibrin: Fibrinolysis/macrophage clearance or fibrous organization.

Pus: Removal of the trigger plus clearance of necrotic material; Possible scarring.

Ulcer: Repair may produce fibrosis, especially with persistent tissue injury.

Fluid → drainage

Fibrin → clear / organize

Pus → clear / scar

Ulcer → heal / scar

Slide 62 · Case comparison: Assign the correct pattern

A burn produces fluid beneath the epidermis → serous.

A pericardial surface is coated by eosinophilic threads → fibrinous.

A focal cavity contains neutrophils and liquefied cell debris → abscess.

A duodenal mucosal crater has an inflamed base → ulcer.

SEROUS

Fluid-rich

FIBRINOUS

Fibrin deposit

PURULENT

Pus + debris

ULCER

Surface defect

Slide 63 · Common interpretive pitfalls

An effusion is not always inflammatory.

Neutrophils are not sufficient to establish an abscess.

Fibrin deposition does not guarantee subsequent fibrosis.

An ulcer is defined by surface tissue loss, not by the presence of pus.

Effusion

Not always inflammation

Neutrophils

Not automatically an abscess

Fibrin

Not always persistent scar

Crater

Defines an ulcer

Slide 64 · Diagnostic integration: Lesion, material, outcome

First locate the lesion relative to a surface, cavity, and surrounding tissue.

Then identify the dominant fluid, extracellular protein, cells, or missing tissue.

Next determine whether necrosis and repair are present.

Finally offer a pattern-based diagnosis with appropriate etiologic caution.

Where is the lesion?

What dominates the exudate?

Is there necrosis / tissue loss?

Is repair occurring?

Slide 65 · Morphologic patterns: Synthesis

Serous = serum-like fluid in a newly created space or mesothelial cavity.

Fibrinous = fibrinogen escape, local coagulation, and fibrin deposition.

Purulent = neutrophils with liquefied necrotic debris; Abscess if localized.

Ulcer = sloughed necrotic surface tissue with an epithelial defect.

SEROUS

Fluid-rich

FIBRINOUS

Fibrin deposit

PURULENT

Pus + debris

ULCER

Surface defect

Slide 66 · References

Robbins, Cotran & Kumar: Pathologic Basis of Disease. 11th edition (2026), Chapter 3: Inflammation and Repair.

Included sections: morphologic patterns; serous, fibrinous and purulent inflammation; abscesses; ulcers; outcomes of acute inflammation.