Chapter 5 Inflammation
AIMS
1. To grasp basic pathological changes of inflammation and characteristics of
acute and chronic inflammation.
2. To be familiar with the sequence of events in inflammation as well as the
structural and molecular mechanisms underlying them, and to be familiar with
systemic effects of inflammation combining with case discussion.
CONTENTS
Gross specimen
Tissue section
Acute severe hepatitis
Acute severe hepatitis
Amoebic abscess of the liver
Epidemic encephalitis B
Serous inflammation
Skin blister
Skin blister
Fibrinous inflammation
Diphtheria
Diphtheria
Bacillary desentery
Bacillary desentery
Fibrinous pericarditis
Fibrinous pericarditis
Alterative inflammation
Exudative inflammation
Lobar pneumonia
Purulent inflammation
Suppurative appendicitis
Phlegmonous appendicitis
Suppurative meningitis
Suppurative meningitis
Abscess of the liver
Abscess of the liver
Abscess of the lung
Abscess of the lung
Abscess of the kidney
Abscess of the kidney
Abscess of the brain
Abscess of the myocardium
Abscess of the cerebellum
Organization of abscess
Phlegmonous inflammation
of the skin
Proliferative inflammation
Non-specific inflammation
Chronic cholecystitis
Chronic cholecystitis
Granulomatous inflammation
Tuberculosis of the lung
Tuberculosis of the lung
Foreign body granuloma
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Inflammatory polyp
Inflammatory polyp of the
intestine
Inflammatory polyp of the
intestine
KEY POINTS OF SPECIMEN OBSERVATION
1. Alterative inflammation
Basic pathologic changes
(1) Gross morphology
◆
Organ presents swollen caused by cell degeneration; or a reduction in volume
owing to massive cellular necrosis.
◆ The
specimen presents necrosis, such as coagulative necrosis, liquefactive necrosis
or gangrene.
(2) Histopathology
◆
Parenchyma cell presents degeneration and/or necrosis, such as hydropic
degeneration, fatty degeneration, coagulative necrosis, and liquefactive necrosis
◆
Mesenchyma cell appears mucoid degeneration or fibrinoid necrosis.
◆
Vessel dilate and inflammatory cell infiltrate.
Specimen observation
(ⅰ) Acute severe viral hepatitis
Case abstract: Male, 45 years old, he suffered fatigue, severe vomit and abdominal
turgor 3 days before, 1 day later he rapidly progressed into anuresis, delirium, marked
confusion and stupor to deep coma. Laboratory examination: electrolyte and acid-base
disturbances, apparently elevated blood ammaonia levels, raising blood urea nitrogen
and creatinine concentration. He died of haematemesis and coma.
Gross specimen: (Fig.5-01) The liver shrinks and is transformed into a limp, red
organ covered by a wrinkled, too-large capsule. On cut surface, necrotic areas have a
muddy red, mushy appearance with blotchy bile staining.
Tissue section: (Fig.5-02a, b)Complete destruction of hepatocytes in contiguous
lobules leaves only a collapsed reticulin framework and preserved portal tracts.
Question: Which basic pathologic changes of inflammation are reflected in this
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lesion?
(ⅱ) Amoebic abscess of the liver
Gross specimen: (Fig.5-03) On the cut surface of the liver, there is a solitary discrete
abscess, 6 cm in diameter. The cavity is filled with some pasty material likened to
anchovy paste, and has a shaggy fibrin lining.
Question: Why does amebic abscess of liver belong to alterative inflammation not
purulent inflammation?
(ⅲ) Epidemic encephalitis B
Case abstract: Female, 4 years old. She suffered from outburst of hyperpyrexia,
twitch, and coma and was dead.
Tissue section: (Fig.5-04a,b,c) What pathologic changes happen in brain tissue?
Which one is dominant?
Question: Why does it belong to alterative inflammation?
2. Exudative inflammation
Basic pathologic changes
(1) Gross morphology
◆
Serous inflammation: Focally inflammatory edema, or hydrops in body cavity.
◆
Fibrinous inflammation: Grayish-white membranous material, pseudomembrane,
appears on the surface of inflamed tissues of the organ (e.g. fibrinous pleurisy);
and Cor Villosum (e.g. fibrinous pericarditis) appears in inflamed pericardium. It
also leads to consolidation in lung.
◆
Purulent inflammation: It shows the production of green-yellow, turbid pus,
consisting of neutrophils, infecting organisms and liquefactive necrosis. Abscess
or empyema or phlegmonous inflammation could be seen..
(2) Histopathology
◆
Blood vessels dilate.
◆
Serous inflammation: Abundant pink protein-rich fluid exudates with relatively
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low cellular content and inflammatory cells.
◆
Fibrinous inflammation: Plentiful fibrinogen containing inflammatory exudates
precipitate to form a tangled threadlike network or sometimes to form as an
amorphous coagulum.
◆
Purulent inflammation: The exudates are composed of large amounts of
neutrophils and pus cells, necrotic tissues, and edema fluid.
Specimen observation
(ⅰ) Skin blister
Gross specimen: (Fig.5-05) Blisters are filled with serous effusion and scattered over
skin surface.
Tissue section: (Fig.5-06) Cross-section of a skin blister shows the epidermis
separated from the dermis by a focal collection of serous effusion, few cells and
fibrin.
Question: In which diseases could this pathological change be presented?
(ⅱ) Diphtheria
Gross specimen: (Fig.5-07a, b)Dissections performed on larynx, bronchus and
trachea all reveal a rough congested mucosa covered by a layer of grayish-white
pseudomembrane. Such membrane adheres tightly on epiglottic and laryngeal regions;
while, it is loosely connected with the sub-mucosa of trachea and bronchus.
Tissue section: (Fig.5-08a,b)Mucosal pseudomembrane is composed of fibrin,
damaged mucosa and neutrophils.
Question: What is pseudomembranous inflammation? What is the difference between
the sequel of laryngeal and tracheal diphtheria lesions?
(ⅲ) Bacillary dysentery
Case abstract: Male, 12 years old. 1 day ago, he ate raw seafood, today complained
of abdominal pain and cramping, diarrhea and tenesmus. Stool examination: loose
stools contain blood, pus and mucus.
Gross specimen: (Fig.5-09a, b) (a)This is a pseudomembranous enterocolitis that
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takes place on the mucosa. The mucosal surface of the colon seen is hyperemic and is
partially covered by whitish-yellow exudates. (b) Bran-like substances surface the
colon mucosal folds, and some fuse into pieces to form grayish-white
pseudomembrane. Mucosa appears thickened due to edema.
Tissue section: (Fig.5-10a, b) Necrosis of colon’s mucosal superficial layer directed
the development of pseudomembrane, a product that constitutes the mixture of
abundant fibrin, mucus, injured tissue, neutrophils, RBC and bacilli. Furthermore,
surrounding mucosa and submucosa become congested and edematous due to
neutrophile and macrophage infiltration.
(ⅳ) Fibrinous pericarditis
Gross specimen: (Fig.5-11a, b, c) (a) Fibrinous exudates are found on the heart
surface. Fine villose form a heavy shaggy coat on the pericardium, results in the “cor
villosum.” The heart is characterized by a rough, ragged appearance and is also
known as the “shaggy heart”. (b) The pericardial cavity has been opened to reveal a
fibrinous pericarditis with strands of stringy pale fibrin between visceral and parietal
pericardium. (c) The epicardial surface of the heart shows a shaggy fibrinous exudate.
This appearance has often been called a "bread and butter" pericarditis.
Tissue section: (Fig.5-12a, b, c) Microscopically, the fibrinous exudates are seen to
consist of pink strands of fibrin jutting from the pericardial surface at the upper right.
Below this, there are a few scattered inflammatory cells. (d) High-power of a
fibrinous pericarditis with a pink meshwork of fibrin exudates, and the fibrinous
exudates are organized by granulation tissue.
Question: How does the cor villosum formed？Which diseases can contribute to cor
villosum？What manifestations could be caused clinically? What are the sequels?
(ⅴ) Lobar pneumonia（see also respiratory system diseases）
(ⅵ) Suppurative appendicitis
Case abstract: Male, 35 years old, he complained of mild fever, nause, and vomit,
and pain, at first periumbilical but then localizing to the right lower quandrant.
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Physical examination: abdomianl tenderness, particularly in the region of the
appendix. WBC: 20×109/L.
Gross specimen: (Fig.5-13a, b, c) (a) Seen here is acute appendicitis with
yellow-white to tan exudates and hyperemia, including the periappendiceal fat
superiorly, rather than a smooth, glistening pale tan serosa surface. The appendix is
swollen. (b) The appendix has been sectioned in half. The serosa surface at the left
shows yellow exudates. The cut surface at the right demonstrates yellowish-tan
mucosal exudation with a hyperemic border. (c) Note the perforation of the appendix.
(ⅶ) Phlegmonous appendicitis
Tissue section: (Fig.5-14a, b, c) (a) Microscopically, the mucosa shows ulceration
and undermining by an extensive neutrophilic exudate. (b)The appendiceal lumen is
filled with pink-stained pus, consisting of living and degenerated neutrophil
polymorphs with liquefied tissue debris. The appendiceal wall is thickened due to a
large number of neutrophils and is noticeably congested, edematous. (c) Neutrophils
extend into and through the wall of the appendix.
Question: What are the clinical manifestations and complications caused by this
lesion?
(ⅷ) Suppurative meningitis
Case abstract: Female, 6 years old. 2 days ago she suffered from headache and
vomiting, suffered coma and was dead. Physical examination: T 40 ℃ ,
unconsciousness and neck stiffness. WBC: 22.5×109/L, N: 0.80. CSF: cloudy,
increased pressure with as many as 3.5×109/L WBC, a raised protein level, and a
markedly reduced glucose content.
Gross specimen: (Fig.5-15a, b) A deposition of viscid, cream-colored suppurative
exudates sits in sub-arachnoid space, especially of the frontal, parietal and occipital
lobes. In severe parts, the exudate obscures the sulci and gyri. Blood vessels on the
cerebral surface are dilated.
Tissue section: (Fig.5-16a, b) Low power view showing inflammatory exudates
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in
the widen subarachnoid space at the depth of a sulcus. The exudates are composed of
plenty of neutrophils, pus cells, a few monocytes and fibrin. The meningeal blood
vessels are engorged extensively. (b) High magnification shows neutrophils and
fibrin.
Question：Which type of purulent inflammation does this specimen belong to？What
are the clinical manifestations and symptoms caused by this lesion?
(ⅸ) Abscess of the liver
Gross specimen: (Fig.5-17) On cut surface of the liver, there is a abscess 6cm in
diameter, the center has whitish-yellow pus formation accompanied by local liver
necrosis, and is walled off by proliferated grayish-white fibrous tissue.
Tissue section: (Fig.5-18) The left part is the abscess infiltrated by large amounts of
neutrophils, some of them undergo degeneration and necrosis. The right part portal
cord could be seen.
(ⅹ) Abscess of the lung
Gross specimen: (Fig.5-19a, b) The abscess is round shaped and about 3 cm in
diameter. The cavity of the abscess in the lower lobe of left lung is filled with pus; it
has a coarse inner surface and is surrounded by fibrous tissues, which formed a thin
suppurative wall. Some suppurative exudates attach to the pleura on the surface of the
abscess. (b) There are rounded abscess cavities formations in the upper and lower
lobes; the purulent material inside has drained out.
Tissue section: (Fig.5-20) This more focal abscess contains a neutrophilic exudate as
well as dark blue bacterial colonies, losing the normal alveolar structure.
Question：What is the difference between early and late stage of abscess wall？
(ⅹⅰ) Abscess of the kidney
Gross specimen: (Fig.5-21) In the lower pole of the kidney is a 1 cm pale yellow
abscess. Infections can reach the kidney either by ascending up the urinary tract (from
a bladder infection, for example) or by hematogenous spread with sepsis. This lone
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abscess was probably hematogenous in origin.
Tissue section: (Fig.5-22a, b) Focal renal tissues are necrotic, and a large quantity of
necrotic neutrophils accumulates. Renal mesenchyma engorgement and edema take
place peripherally to the abscess.
(ⅹⅱ) Abscess of the brain
Gross specimen: (Fig.5-23) On the cut surface of the brain, there is a round abscess
2.5cm in diameter situated in the occipital lobe, and it is filled with some
yellowish-white pus. The abscess is demarcated by thick fibrous wall.
(ⅹⅲ) Abscess of the cerebellum
Gross specimen: (Fig.5-24) Please describe by yourself.
(ⅹⅳ)Abscess of myocardium
Tissue section: (Fig.5-25) Seen here is a micro-abscess in the myocardium. There are
localized collections of neutrophils in alveolar cavity. The irregular dark purple center
is a collection of bacteria that are the cause for this abscess.
(ⅹⅴ)Organization of abscess
Tissue section: (Fig.5-26a, b) (a) The wall of an abscess that is organizing has
granulation tissue, seen here at the left. The purulent exudate with some hemorrhage
is seen at the right in the abscess center. (b) The abscess has a mixture of
inflammatory cells, but the wall of the abscess is "organizing" with ingrowth of
capillaries and fibroblasts (granulation tissue).
(ⅹⅴⅰ) Phlegmonous inflammation of the skin
Gross specimen: (Fig.5-27) Epidermis exfoliated with whitish-yellow purulent
exudates is present in the subcutaneous tissue. The lesion appears diffused with
unclear boundary and the dermis is clearly thickened.
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Question：Which tissue or organ does this lesion usually happen？What is the
difference between phlegmonous inflammation and abscess？
3. Proliferative inflammation
Basic pathologic changes
(1) Gross morphology
◆
The commonest appearance of non-specific proliferative inflammation are
thickening of the wall of a hollow viscus and fibrosis. Inflammatory polyp or
inflammatory pseudotumor sometimes could be seen.
◆
Granulomatous inflammation appears well-circumscribed tuberculous focus
formation.
(2) Histopathology
◆
The commonest features of non-specific proliferative inflammation are : ①
Infiltration of lymphocytes, mononuclear and plasma cells; ② Proliferation of
vascular endothelial cells, fibroblasts and parenchyma cells; ③ Connective
tissue replacement of damaged tissue, accomplished by proliferation of small
blood vessels and fibrosis.
◆
The commonest feature of granulomatous inflammation is granuloma formation, it
consists of a microscopic aggregation of macrophages that are transformed into
epithelium-like cells surrounded by a collar of mononuclear leukocytes,
principally lymphocytes and occasionally plasma cells. The foreign material or
necrosis can be identified in the center of the granuloma.
Specimen observation
(ⅰ) Chronic cholecystitis
Gross specimen: (Fig.5-28) The gallbladder mucosa is coarse and the wall is
thickened by fibrous tissue.
Tissue section: (Fig.5-29) Please describe by yourself.
(ⅱ) Pulmonary miliary tuberculosis (see also chapter 15)
Gross specimen: (Fig.5-30) There are a multitude of small, round, slightly protruded,
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tan granulomas, about 2 to 4 mm in size, scattered throughout the lung parenchyma.
Tissue section: (Fig.5-31a, b, c) The tuberculous granuloma (tubercle) shows an area
of central caseous necrosis, plenty of epithelioid cells, Langhans-type giant cells and
lymphocytes.
The caseous necrotic focus appears as pink, amorphous granular debris, loss of all
cellular detail. (d) The epithelioid cells have a pale pink granular cytoplasm with
indistinct cell boundaries; nuclei tend to be long and stringy.
Epithelioid cells fuse to form Langhans giant cells containing 20 or more small
nuclei arranged either peripherally (Langhans-type giant cell) or haphazardly (foreign
body type giant cell).
(ⅲ) Foreign body granuloma
Tissue section: (Fig.5-32) Two foreign body giant cells are seen just to the right of
center where there is a bluish strand of suture material from a previous operation, and
there are also macrophages, fibroblasts.
Question: Morphologically what is the difference of foreign body giant cell and
Langhans-type giant cell?
(ⅳ) Inflammatory polyp of intestine
Gross specimen: (Fig.5-33) Smooth mass of tissue (polyp) with stalks protrudes
outwards from the surface of intestinal mucosa.
Tissue section: (Fig.5-34) Mucosal epithelium, gland and granulation proliferate, and
there are lymphocyte and plasma cell infiltration.
Question：Please describe the process of polyp formation. What kind of inflammation
does it belong to？
CASE DISCUSSION
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Clinical case
Case abstract. A forty-year old male suffered from furuncle of the neck，the patient
experienced localized redness, swelling, pain and heat. Ten days later, local redness
and swelling expanded to the size of a palm and body temperature measured to be
38℃. Surgical procedures (dissection and drainage) were performed on the swelling
furuncle, later that night the patient felt shivery, fever and headache. On the following
day, physical examination showed mild jaundice, swelling of the liver and the spleen,
WBC 21×109/L and body temperature was 39℃.
Discussion
To make a pathologic diagnosis of the case and to explain the above clinical
manifestations using learned knowledge on acute inflammation.
Autopsy case
Case abstract. Female, 62 year-old, was admitted to the hospital for emergency care
of fever and upper abdominal pain that lasted for 3 days.
Current Case abstract. Two days ago, the patient experienced upper abdominal pain
and a fever of 38.8℃. Anti-inflammation treatment received at a local hospital turned
out to be inadequate. On the third day, the patient was inhospitalized due to the
deterioration of above mentioned symptoms, multiple vomits, and listlessness.
Past Case abstract. Diabetes for 7 years, gallstones for 2 years.
Physical examination. The patient behaved apathetically，body temperature was
38.2℃ and BP12.0/8.0kpa. Mild jaundice of the sclera and peripheral regions of the
skin, swollen lymph nodes of the neck, clear auscultation of the lung bilaterally, heart
rate 120/min，weak heart sound，sub-xiphoid and upper right abdominal pain(+),and
unsatisfactory palpation of the liver and spleen.
Laboratory diagnosis. WBC 28.4×109/L，bacillary nucleus 9％，polymorphic
nucleus80％. Hepatic-splenic ultrasound：enlarged liver and spleen, dilation of
intra-hepatic bile ducts, gallstone formed.
Clinical
diagnosis.
① Acute
cholecystitis,
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cholethiasis ？ ② Suppurative
cholangitis？③Septicemia，inflammatory shock？④TypeⅡdiabetes.
Treatment. Alimentary decompression, anti-inflammation and anti-shock were
performed. Treatments were ineffective and the patient died 2 days later.
Autopsy records
Skin：Mild jaundice.
Lymph node：Lymph nodes of the neck and groin are swollen.
Heart：270g.Tissue slice：Myocardial cells are degenerated and necrosis.
Liver: 1800g. Increased in size，the edges are obtunded, cut edge turned inside out, its
color became pale and cloudy. Bile duct dilated, whitish-yellow pus accumulated in
the cavity.
Spleen: 220g. Capsule ruffled with soft sensation. Under light microscope:
macrophage proliferated, sinal endothelial cells are swollen and exfoliated, and
macrophages and a few neutrophils are present inside the splenic sinus.
Kidney: 185g. Increased in size, cut face protruded, cut edge turned inside out, the
color became pale and cloudy (Fig.5-35). Light microscope: (Fig.5-36) what
pathological changes can be seen microscopically? Please describe by yourself.
Discussion
1. What lesions are there in this case according to autopsy specimens and tissue
slides? What correlation is there among these lesions？
2. To analyze the correlation of lesions and clinical manifestations.
3. To analyze the cause of death in the patient.
PRACTICE REPORT
1. Illustrate the histological morphology of ① Fibrinous pericarditis; ②
Myocardium abscess.
2.
Describe the pathologic characteristics of phlegmonous inflammation.
3.
Write out the outline of case discussions.
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QUESTIONS FOR REVIEW
1. How to diagnose inflammation pathologic morphologically？
2. What characteristics posed by all exudative inflammations have in common
under light microscope? What are the differences in clinical symptoms among
different types of exudative inflammations?
3. Compare the following pairs based on the morphology and sequel of lesions
(1) Fibrinous inflammation in mucosa versus in serosa.
(2) Abscess versus phlegmonous inflammation.
(3) Acute inflammation versus chronic inflammation.
(China Medical University Han Yuchen, Qiu Xueshan)
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