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CHAPTER 15 Disorders of Growth, Morphogenesis and Differentiation
301
BOX 15.2 Teratogens and Their Effects
Teratogen Teratogenic Effect
Irradiation Microcephaly
Drugs
Thalidomide Amelia/phocomelia (absent/rudimentary limbs; heart, kidney,
gastrointestinal and facial abnormalities)
Folic acid antagonists, e.g. 4 amino PGA Anencephaly, hydrocephalus, cleft lip/palate, skull defects
Anticonvulsants Cleft lip/palate, heart defects, minor skeletal defects
Warfarin Nasal/facial abnormalities
Testosterone and synthetic progestogens Virilization of female fetus, atypical genitalia
Alcohol Microcephaly, abnormal facies, oblique palpebral fissures, growth
disturbance
Infections
Rubella Cataracts, microphthalmia, microcephaly, heart defects
Cytomegalovirus Microcephaly
Herpes simplex Microcephaly, microphthalmia
Toxoplasmosis Microcephaly
• Failure of cell and organ maturation, e.g.
• Kartagener’s syndrome: defect in ciliary motility
aects cell mobility during organogenesis, resulting
in situs inversus; in later life results in bronchiectasis
and infertility (due to sperm immobility)
• Hirschsprung’s disease: absence of ganglion cells in
Meissner’s and Auerbach’s plexuses due to defective
migration of cells from neural crest
• undescended testis (cryptorchidism): oen isolated
anomaly, but may be associated with Klinefelter’s
syndrome.
Anomalies of Organogenesis
ese include:
• agenesis: failure of development of an organ or structure
• atresia: failure of development of a lumen in a normally
tubular structure
• hypoplasia: failure of an organ to attain its normal size
• dysgenesis: failure of normal organ dierentiation or
persistence of primitive embryological structures
• ectopia: development of mature tissue at an inappropriate site.
Agenesis (Aplasia)
• Renal agenesis:
• may be unilateral or bilateral
• failure of mesonephric duct to give rise to ure-
teric bud, with failure of induction of metanephric
blastema.
• ymic agenesis (di George syndrome):
• resulting in absent T-cells and deciency of cellmediated immunity.
• Anencephaly:
• absence of cerebrum due to neural tube defect; fatal.
Atresia
• Oesophageal atresia:
• failure of separation of trachea and oesophagus from
primitive foregut
• may be associated with tracheo–oesophageal stula.
• Biliary atresia:
• absence of bile ducts; obstructive jaundice in infancy.
Hypoplasia
• Developmental dysplasia of the hip.
• failure of development of bone of acetabulum, causing
dislocation of hip due to attened acetabular roof.
Dysgenesis (Dysplasia)
• Renal dysgenesis due to anomalous metanephric dierentiation.
Ectopia (Heterotopia)
• Gastric mucosa in a Meckel’s diverticulum.
Acquired Disorders of Differentiation and Growth
ese include:
• metaplasia
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SECTION III Pathology
• dysplasia
• polyps
• neoplasia.
Metaplasia
Metaplasia is the reversible transformation of one type of
terminally dierentiated cell into another fully dierentiated cell type.
Metaplasia:
• may aect epithelial or mesenchymal cells
• oen represents an adaptive response of tissues to environmental stress
• is due to activation and/or repression of genes involved
in maintenance of cellular dierentiation
• metaplastic tissue is better able to withstand adverse
environmental changes
• itself does not progress to malignancy, but may under go further indirect transformation to neoplasia via
dysplasia.
Examples of metaplasia in epithelial tissue include:
• squamous metaplasia in ciliary epithelium of bronchus
in smokers
• squamous metaplasia in transitional epithelium in the
bladder in schistosomiasis
• replacement of squamous epithelium in the oesophagus
with columnar glandular epithelium in patients with
reux (Barrett’s oesophagus)
• transformation of the columnar lining of the gall bladder to squamous epithelium in the presence of gallstones and chronic inammation
• squamous metaplasia in the nose, bronchi and urinary
tract associated with vitamin A deciency.
Examples of metaplasia in mesenchymal tissues include:
• bone formation (osseous metaplasia):
• calcium deposition in atheromatous arterial walls
• in bronchial cartilage.
• Cellular atypia:
• pleomorphism
• high nuclear–cytoplasmic ratio
• hyperchromatic nuclei (denser staining due to
increased nuclear DNA).
• Decreased cellular dierentiation:
• cells more primitive than normal.
Other features of dysplasia:
• May be present for many years before malignancy
develops.
• May occur in tissue which has coincidental metaplasia, e.g.
• dysplasia in metaplastic squamous epithelium in the
bronchus of smokers
• dysplasia in metaplastic glandular epithelium in
Barrett’s oesophagus.
• May develop without coexisting metaplasia, e.g.
• squamous epithelium of uterine cervix
• glandular epithelium of the stomach.
Polyps
A polyp is a sessile or pedunculated protrusion from a body
surface.
Polyposis is a term used to describe a condition or syn-
drome where there are multiple polyps in an organ or organ
system, e.g.
• organ: polyposis coli of large bowel
• organ system: Peutz–Jeghers syndrome: hamartomatous polyps throughout the gastrointestinal tract.
e term polyp:
• is purely descriptive of the shape of a lesion
• does not imply any specic underlying pathological
process, e.g. hyperplasia, neoplasia
• is a result of focal tissue expansion at a site, at or near
a body surface, which, when enlarging, takes the line
of least resistance, i.e. outwards to a surface or lumen
rather than inwards.
Dysplasia
Dysplasia is a premalignant condition characterized
by increased cell growth, cellular atypia and decreased
dierentiation.
Dysplasia:
• may be caused by long-standing irritation of tissues by
chronic inammation or exposure to carcinogens
• in the early phases may be reversible if the initial stimulus is removed
• if severe, will progress to malignancy unless adequately
treated.
Dysplasia may be recognized by:
• Evidence of increased growth:
• increased tissue bulk
• increased mitotic activity.
Pathological Processes Causing Polyps
ese may be either non-neoplastic or neoplastic.
• Non-neoplastic:
• inammation
• hyperplasia
• metaplasia
• dysplasia.
• Neoplastic:
• epithelial
• mesenchymal
• lymphoid.
Non-neoplastic and most neoplastic polyps are common
and benign, but a small proportion of malignant neoplasms
have a polypoid appearance, e.g. polypoid adenocarcinoma
of the colon, lymphomatous polyps of GI tract.
CHAPTER 15 Disorders of Growth, Morphogenesis and Differentiation
303
Symptoms of Polyps
Polyps may be asymptomatic or may produce symptoms:
• haemorrhage
• local trauma
• torsion
• inammation
• ulceration
• anaemia:
• ulceration
• mechanical eects:
• obstruction
• intussusception.
Examples of Polyps
Polyps occur in many organ systems. Accurate diagnosis
is essential and histopathological examination is required
to determine a precise pathological diagnosis. Examples of
polyps include:
• Nasal:
• very common
• due to chronic infective or allergic inammation
• consist of oedematous masses of connective tissue
with inammatory cells and glands.
• Uterine (endometrial):
• hyperplastic/metaplastic polyps
• found in perimenopausal women
• caused by inappropriate response of endometrium to
oestrogenic stimuli
• malignant change is rare.
• Uterine (cervical):
• epithelial non-neoplastic polyps
• common
• consist of columnar mucus-secreting epithelium
with oedematous stroma
• no malignant potential.
• Colonic:
• the large bowel is by far the most common site for
gastrointestinal polyps. Types of polyps occurring in
the large intestine are shown in Table 15.1.
Neoplasia
Neoplasia have the following characteristics:
• abnormal and excessive cell growth uncoordinated with
that of normal tissues
• persist aer the initiating stimulus has been withdrawn
• associated with genetic alteration
• influence behaviour of normal cells by production
of hormones (a paraneoplastic effect) and growth
factors.
Neoplasia are covered in detail in Chapter 18.
TABLE 15.1 Polyps of the Large Intestine
Type Benign Malignant
Epithelial Neoplastic Adenocarcinoma
• adenoma Carcinoid
• tubular adenoma
• tubulo-villous adenoma
• villous adenoma
Inflammatory
• pseudopolyp, e.g. ulcerative colitis
Hamartomas
• juvenile polyp
• Peutz–Jeghers syndrome
Metaplastic
• adenoma
Mesenchymal Lipoma Sarcomas
Leiomyoma Lymphomatous polyps
Fibromas
Haemangiomas
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SECTION III Pathology
OSCE SCENARIOS
OSCE Scenario 15.1
A 66-year-old male is admitted through A&E with painless
red bleeding per rectum. He has no past medical history
and a subsequent colonoscopy shows multiple benignlooking polyps only, which have been biopsied. He is anxious and worried about his condition and has asked to
speak to a doctor.
1. Answer the patient’s questions about polyps and rectal
bleeding. Explain the dierent types of polyps and the
need for the biopsy, avoiding medical jargon.
e patient then explains that several members of his family have had ‘camera tests’ in their bowel, and you notice
some small dark dots on his lower lip.
2. Name the most likely condition causing this patient’s
polyps.
3. Explain to the examiners the type of polyps caused
by this condition, any risks from the polyps and any
screening procedures that need to be in place.
OSCE Scenario 15.2
A 40-year-old-male presents to your orthopaedic outpatient
clinic having been referred by his GP for ‘tingling’ sensations in his hands. He complains of the symptoms progressing over the last nine months. He is a carpenter by trade
and is starting to drop things due to weakness in his grip.
He has no past medical history and takes no medications.
He is concerned about his hands, as being self-employed his
inability to work is impacting upon him nancially.
1. Take a brief history regarding this patient’s symptoms
and examine his hands.
2. What is the diagnosis?
e patient then explains that he has seen his GP for headaches recently, which he feels are stress-related due to his
worry about his job.
3. In view of this new information and your previous diag-
nosis, what condition are you now concerned about?
4. Explain to the examiners the other symptoms and signs
you would now check for in this patient, and briey out-
line the investigations and management.
OSCE Scenario 15.3
A nurse in your clinic asks you to see a very distressed
50-year-old gentleman regarding the result of a biopsy
performed on his cheek two weeks ago. He attended the
outpatient clinic earlier today, and was informed by a different doctor that he had ‘dysplasia’ ‘but it was completely
removed and nothing to worry about’ and was told to come
back in three months. He has spent the last two hours near
to tears in the hospital canteen and tells you he is worried
he has cancer.
1. Explain the diagnosis of dysplasia to this gentleman,
being sensitive to his heightened emotional state.
2. Tell the examiners what risk factors exist for oral cav-
ity tumours and the names of any pre-malignant conditions you know of.
3. How would you draw this consultation to a close and
ensure the patient felt supported?
OSCE Scenario 15.4
A 35-year-old man with a long-standing history of gastrooesophageal reux undergoes endoscopy which reveals
suspicion of Barrett’s oesophagus. Biopsy conrms the diagnosis, and the patient attends outpatient clinic to discuss
the results.
1. Describe to the patient the diagnosis and pathogenesis.
2. What is the signicance of Barrett’s oesophagus?
3. e patient does not attend any further medical appoint-
ments and aer 15 years presents with history of dysphagia and weight loss. Investigations reveal advanced
lower oesophageal cancer. Palliative chemotherapy is
advocated. Describe the phases of cell cycle and the relationship to chemotherapy.
4. As you discuss potential side eects of chemotherapy,
explain to the patient the reason for the likelihood of
hair loss, developing anaemia and the susceptibility to
infection and bleeding.
OSCE Scenario 15.5
A 15-year-old boy attends the outpatient clinic with his
parents aer getting concerned regarding bilateral breast
enlargement over the past year. is is causing embarrassment and he would like to understand its aetiology.
Following assessment, you conclude that the ndings are
consistent with physiologic changes during puberty.
1. Explain to the patient and his family the underlying
pathogenesis.
2. Give other examples of organs that can undergo physi-
ologic changes during early adulthood.
3. What are the other causes of gynaecomastia that you
need to exclude?
Answers in Appendix pages 464–467
Please check your eBook at https://studentconsult.inkling.com/ for more self-assessment questions. See inside cover for
registration details.
16
Inflammation
Inammation is the local physiological response to injury.
CLASSIFICATION
• Acute inammation: the initial and oen transient reaction to injury.
• Chronic inammation: the subsequent and oen prolonged tissue reaction to injury.
Acute Inflammation
• Vascular phase:
• change in vessel calibre
• increased vascular permeability
• formation of uid exudates.
• Exudative cellular phase:
• adhesion of neutrophils
• neutrophil migration
• diapedesis
• neutrophil chemotaxis.
• Outcome:
• resolution
• suppuration
• organization
• chronic inammation.
Causes of Acute Inflammation
• Microbial infections:
• pyogenic bacteria
• viruses.
• Hypersensitivity reactions:
• parasites
• tubercle bacilli.
• Chemical agents:
• corrosives
• acids
• alkalis
• toxins.
• Physical agents:
• trauma
• ionizing radiation
• heat
• cold.
• Tissue necrosis:
• ischaemia
• infarction.
Macroscopic Signs and Symptoms of
Acute Inflammation
• Redness (rubor):
• small vessel dilatation.
• Heat (calor):
• increased blood ow in skin.
• Swelling (tumour):
• oedema.
• Pain (dolor):
• stretching and tissue distortion
• pus under pressure in abscess
• chemical mediators, e.g. prostaglandins, bradykinins.
• Loss of function (functio laesa):
• conscious and reex inhibition of movement by pain
• swelling may physically immobilize tissues.
Stages of Acute Inflammation
• Change in vessel calibre.
• Increased vascular permeability.
• Formation of cellular exudates.
Changes in Vessel Calibre
• Changes described by Lewis in 1927 as ‘triple response
to injury’: ush, are, weal.
• If a blunt instrument is drawn across the skin the following changes take place:
• transient white line due to arteriolar vasoconstriction
• ush: dull red line due to capillary dilatation
• are: red irregular zone due to arteriolar dilatation
• weal: zone of oedema due to uid exudate in to the
extravascular space.
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SECTION III Pathology
Increased Vascular Permeability
• Capillary hydrostatic pressure increased in acute in ammation.
• More uid leaves vessels than returns to them.
• Formation of an exudate: a protein-rich uid.
• Fluid exudates:
• protein content up to 50 g/L
• contains immunoglobulins: destruction of invading
micro-organisms
• coagulation factors: brinogen converted to brin in
brinous exudates.
• Removal of exudate by lymphatic channels and replacement with new exudate if stimulus to inammation
persists.
Formation of Cellular Exudate
• Margination of neutrophils.
• Neutrophil adhesion:
• interaction between paired adhesion molecules on
leucocyte and endothelial surfaces
• leucocyte surface adhesion molecule expression
increased by:
• complement C5a
• leukotriene B4
• tumour necrosis factor (TNF).
• endothelial expression of adhesion molecules
increased by:
• interleukin-1 (IL-1)
• endotoxins
• TNF.
• Neutrophil migration.
• Amoeboid movement through venules (C5a and leukotriene B4).
• Diapedesis:
• escape of red cells from capillaries
• passive; depends on hydrostatic pressure.
• Neutrophil chemotaxis:
• leukotriene B4
• IL-8.
Chemical Mediators of Acute Inflammation
• Histamine:
• source: mast cell, basophil, eosinophil, platelets
• release stimulated by C3a, C5a, neutrophil lysosomal
protein
• action: vasodilatation transiently increases vascular
permeability.
• Lysosomal compounds:
• source: neutrophils
• release stimulated by bacteria, damaged tissue
• action: increased vascular permeability
• activate complement.
• Prostaglandins:
• source: platelets, endothelium, monocyte/macrophage, other cells
• action: dierent actions:
• potentiate increase in vascular permeability
• platelet aggregation (pA2)
• platelet disaggregation (pI2).
• Leukotrienes:
• synthesized from arachidonic acid
• synthesis occurs in neutrophils, mast cells, basophils,
some macrophages
• SRS-A (slow reacting substance of anaphylaxis) is
a mixture of leukotrienes involved in type I hyper sensitivity.
• Cytokines:
• source: many cells
• action: attract various types of leucocyte to site of
inammation, e.g. IL-8 mainly specic for neutrophils.
• Nitric oxide:
• source: endothelium, macrophage, short-lived free
radicals
• action: toxic to bacteria; major factor in endotoxic
shock.
Plasma Factors
• Complement.
• Kinins.
• Coagulation system.
• Fibrinolytic system.
Complement System
• Cascade of enzymatic proteins.
• Series of 20 proteins synthesized in liver and macrophages.
• Activated during acute inammatory response:
• enzymes released from dying cells during tissue
necrosis
• infection
• products of kinins, coagulation and brinolytic system.
• Products of complement activation important in inammation are:
• C5a: chemotactic for neutrophils; increase vascular
permeability, release of histamine from mast cells
• C3a: similar action to C5a but less active
• C5, 6, 7: chemotactic for neutrophils
• C5, 6, 7, 8, 9: cytolytic activity
• C4b, 2a, 3b: opsonization of bacteria and facilitate
phagocytosis by macrophages.
Kinin System
• Activated by coagulation factor XII.
• Converts prekallikrein to kallikrein.
CHAPTER 16 Inflammation
307
• Kallikrein cleaves kininogen to release bradykinin.
• Bradykinin controls vascular permeability and is a
chemical mediator of pain.
Coagulation System
• Protein synthesized in liver in inactive form.
• System responsible for conversion of brinogen to brin,
a major component of the inammatory response.
• Coagulation factor XII is activated by exposed basement membranes and various proteolytic enzymes of
bacterial origin. In turn it activates coagulation, kinin
and brinolytic systems.
Fibrinolytic System
• Protein synthesized in liver.
• Negative feedback arm that limits coagulation.
• Plasmin (released by action of activated factor XII),
lyses brin to brin degradation products (FDP).
Role of Macrophages
• Stimulated by local infection or injury.
• Produce IL-1 and TNF-α which stimulate endothelial
cells to produce adhesion molecules which bind and
activate neutrophils.
Role of Lymphatics
Terminal lymphatics are blind-ended endotheliumlined tubes present in most tissues in similar numbers to
capillaries.
• Lymphatics drain into collecting lymphatics, which
have valves and propel lymph passively to lymph nodes.
• Gaps open passively between lymphatic endothelial cells,
allowing large protein molecules to enter.
• In acute inammation lymphatic channels become
dilated as they drain away oedema uid of inammatory exudates.
• is tends to limit the extent of tissue oedema.
• Important in the immune response to infecting agents
as antigens are carried to regional lymph nodes for recognition by lymphocytes.
Role of Neutrophil Polymorphs
• Characteristic cell of acute inammatory exudates.
• Movement: amoeboid movement in a directional response
(chemotaxis) to chemicals of acute inammation.
• Bind to micro-organisms which have been opsonized by
immunoglobulins or complement components.
• Phagocytosis: facilitated by opsonization. Cells ingest
particle into vacuole, which fuses with lysosome, resulting in killing of micro-organism.
• Release of lysosomal products: damage local tissues by
proteolysis, e.g. elastase and collagenase. Some compounds
released increase vascular permeability, while others are
pyrogens causing systemic fever.
SPECIAL TYPES OF INFLAMMATION
1. Serous
• Abundant protein-rich uid with low cellular content.
• Inammation of serous cavities, e.g. peritonitis (peritoneal cavity), synovitis (synovial joint).
• Vascular dilatation apparent to naked eye, e.g. conjunctivitis.
2. Catarrhal
• Hypersecretion of mucus in acute inammation of a
mucous membrane, e.g. coryza (common cold).
3. Fibrinous Inflammation
• Exudate contains much brinogen.
• Fibrin forms a thick coating, e.g. acute pericarditis,
brinous peritonitis.
4. Haemorrhagic Inflammation
• Accompanied by vascular injury or coagulopathy.
• Examples include acute haemorrhagic pancreatitis due
to proteolytic digestion of vessel walls; and meningococcal septicaemia, resulting from associated disseminated intravascular coagulation (DIC).
5. Suppurative Inflammation
• Production of pus, i.e. dying and degenerate neutrophils, organisms and liqueed tissues.
• May become walled-o by brin or brous tissue to
produce an abscess, i.e. a localized collection of pus.
• May form an empyema (a collection of pus in a hollow
viscus, e.g. gall bladder).
6. Membranous Inflammation
• Epithelium coated with a membrane of brin, desquamated epithelial cells and inammatory cells.
• Example: grey membrane seen in pharyngitis due to
diphtheria.
7. Pseudomembranous Inflammation
• Supercial mucosal inammation and ulceration with
sloughing of mucosa, brin, mucus and inammatory
cells.
• Example: pseudomembranous colitis due to Clostridium
difficile.
8. Necrotizing Inflammation
• Tense oedema may cause vascular occlusion and thrombosis, resulting in septic necrosis.
• Example: gangrenous appendicitis.
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SECTION III Pathology
Effects of Acute Inflammation
Beneficial Effects (Exudate)
• Dilution of toxins.
• Arrival of antibodies.
• Transport of drugs.
• Fibrin formation.
• Delivery of oxygen and nutrients.
• Stimulation of immune response.
Harmful Effects (Release of Lysosomal Enzymes)
• Digestion of normal tissue.
• Swelling.
• Inappropriate inammatory response, e.g. type I hypersensitivity reactions.
Sequelae of Acute Inflammation
• Resolution.
• Suppuration.
• Organization.
• Chronic inammation.
Resolution
• Resolution is complete restoration of tissues to normal.
Conditions favouring resolution
Include:
• Minimal tissue damage.
• Occurrence in organ with regenerative capacity, e.g.
liver, rather than one that cannot regenerate, e.g. brain.
• Rapid destruction of causal agents, e.g. bacterial
phagocytosis.
• Rapid removal of uid and debris.
Sequence of events leading to resolution
• Phagocytosis of bacteria.
• Fibrinolysis.
• Phagocytosis of debris by macrophages.
• Resolution of vascular dilatation.
Suppuration
• e formation of pus.
• Pus is a mixture of living, dead and dying bacteria and
neutrophils with cellular debris and liqueed tissue.
• e causative organisms are usually pyogenic bacteria,
e.g. Staphylococcus aureus, Staph. pyogenes, coliforms
and Neisseria spp.
• e causative stimulus is usually persistent.
• An accumulation of pus in the tissues becomes surrounded by a ‘pyogenic membrane’, i.e. capillaries, neutrophils and occasional broblasts.
• Bacteria within abscess cavities are relatively inaccessible
to antibiotics and antibodies; hence the need to drain pus.
Organization
• Organization is replacement of the tissue by granulation
tissue.
Circumstances favouring organization
• Excess brin formation with swamping of the brinolytic system.
• Substantial volume of necrotic tissue.
• Exudate and debris cannot be removed or discharged.
Sequence of organization
• Capillaries grow into the inammatory tissue.
• Fibroblasts proliferate under the inuence of TGF-β,
resulting in brosis.
• Example: aer peritonitis a brinous exudate covers the
bowel and loops stick together in a brinous adhesion.
Failure to remove the brin results in its invasion with
capillaries accompanied by broblasts, which lay down
collagen resulting in a permanent brous adhesion
between loops of bowel.
Progress to Chronic Inflammation
• Acute inammation may progress to chronic if the causative agent is not removed.
• e tissues become organized and the cellular exudate
changes with lymphocytes, plasma cells and macrophages,
and multinuclear giant cells replacing polymorphs.
Systemic Effects of Inflammation
• Pyrexia.
• Weight loss.
• Constitutional symptoms, e.g. malaise, nausea, anorexia.
• Haematological changes:
• increased ESR
• leucocytosis.
• Reactive hyperplasia:
• lymphadenopathy
• splenomegaly.
• Anaemia:
• loss of blood into exudates, e.g. acute pancreatitis
• haemolysis, e.g. bacterial toxin
• ‘anaemia of chronic disease’ – bone marrow
depression.
• Amyloidosis (secondary or reactive):
• long-standing chronic inammation, e.g. TB, rheu-
matoid arthritis, bronchiectasis.
CHRONIC INFLAMMATION
Chronic inammation implies that the process has
extended over a long period of time; however, the term
‘chronic’ applied to inammation indicates a cellular inltrate that diers from acute inammation, i.e. lymphocytes,
CHAPTER 16 Inflammation
309
plasma cells and macrophages predominate in chronic
inammation. Chronic inammation is usually primary
but occasionally follows acute inammation.
Features of Chronic Inflammation
• Lymphocytes, plasma cells and macrophages predominate.
• Usually primary but may follow acute inammation.
• Granulomatous inammation is a specic type of
chronic inammation.
• May be complicated by secondary amyloidosis.
Causes of Chronic Inflammation
• Primary chronic inammation.
• Progress from acute inammation.
• Recurrent episodes of acute inammation.
• Transplant rejection.
Primary Chronic Inflammation
• Resistance of infective agents to phagocytosis and intracellular killing, e.g. tuberculosis, leprosy, viral infections.
• Foreign body reactions:
• endogenous materials, e.g. necrotic bone, uric acid
crystals
• exogenous materials, e.g. asbestos bres, suture
materials, implanted prostheses.
• Autoimmune diseases, e.g. Hashimoto’s thyroiditis,
chronic gastritis of pernicious anaemia, rheumatoid
arthritis.
• Specic diseases of unknown aetiology, e.g. chronic
inammatory bowel disease – ulcerative colitis.
• Primary granulomatous disease, e.g. Crohn’s disease,
sarcoidosis.
Progression from Acute Inflammation
• Commonest variety of acute inammation to progress
to chronic inammation is the suppurative type.
• Inadequate drainage of pus which is deep-seated, e.g.
chronic abscess of osteomyelitis or chronic empyema
thoracis.
• Foreign-body reactions may develop into granulomatous reactions, e.g. suture material, wood, metal, glass,
implanted prosthesis.
Recurrent Episodes of Acute Inflammation
• Recurring cycles of acute inammation and healing
eventually result in chronic inammation.
• Best example of this in clinical practice is chronic cholecystitis due to gallstones. Multiple recurrent episodes
of acute inammation lead to replacement of the gall
bladder muscle with brous tissue.
Transplant Rejection
• Cellular rejection of renal transplants involves chronic
inammatory cell inltration.
Macroscopic Appearances of Chronic
Inflammation
• Chronic ulceration:
• venous stasis ulcer
• peptic ulcer.
• Chronic abscess:
• osteomyelitis.
• Caseating granulomatous inammation:
• pulmonary tuberculosis.
• ickening of a hollow viscus:
• chronic cholecystitis
• Crohn’s disease.
• Fibrosis:
• distortion, e.g. pyloric stenosis aer peptic ulceration.
GRANULOMATOUS DISEASE
A granuloma is an aggregate of epithelioid histiocytes.
Epithelioid histiocytes
• Named because of vague histological resemblance to
epithelial cells.
• Arranged in clusters.
• Little phagocytic activity.
• Produce angiotensin-converting enzyme (raised in
sarcoidosis).
• Caseous necrosis may occur in granulomas, e.g. tuberculosis.
• Histiocytes may be converted into multinucleate giant
cells.
Types of Giant Cell
• Histiocytic:
• form where particulate matter is indigestible by mac-
rophages, e.g. silica, tubercle bacilli.
• Langhans:
• horseshoe arrangement of peripheral nuclei at one
pole of cell
• characteristically seen in tuberculosis.
• Foreign body:
• large cells with nuclei randomly scattered through-
out cytoplasm
• seen in relation to particulate foreign body material.
• Touton:
• ring of central nuclei
• clear peripheral cytoplasm with accumulated lipid, seen
at sites of adipose tissue breakdown and in xanthomas.
310
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SECTION III Pathology
Causes of Granulomatous Disease
• Specic infections:
• mycobacteria, e.g. tuberculosis
• fungi
• parasites.
• Foreign bodies:
• endogenous, e.g. keratin, necrotic bone, uric acid
crystals
• exogenous, e.g. talc, silica, suture materials, silicone.
OSCE SCENARIOS
OSCE Scenario 16.1
A 16-year-old male presents to your clinic with a 6-month
history of weight loss and vague abdominal pain with intermittent rectal bleeding.
1. Outline your history, examination and investigations.
2. What is your dierential diagnosis?
e colonic mucosal biopsy shows chronic inammation with focal colitis and granulomas. e patient is
currently well but is worried as he does not know what
this means.
3. Explain the ndings and diagnosis to the patient.
OSCE Scenario 16.2
A 19-year-old male is admitted with a history of central
abdominal pain localizing to the right iliac fossa aer 12 h.
It is now ve days since the onset of symptoms. On admission to A&E he has a temperature of 38.5°C with a tachycardia of 120, and abdominal examination reveals a tender
mass in the right iliac fossa. A clinical diagnosis of appendix abscess is made and this is conrmed by CT scan.
1. What is suppuration? Why in some cases does acute
appendicitis perforate and cause peritonitis while in
others abscess formation occurs?
2. Why do abscesses require drainage?
3. What organisms are likely to be cultured from the pus?
4. What sequelae other than suppuration may follow acute
inammation?e patient is re-admitted to hospital 1
year later with vomiting, central abdominal colicky
pain, abdominal distension and constipation. Plain
abdominal X-ray shows dilated loops of small bowel
and a diagnosis of small bowel obstruction is made.
5. Why is this likely to have occurred? Explain the pathol-
ogy of the condition.
OSCE Scenario 16.3
You see an 8-year-old girl along with her mother in A&E
who fell over earlier today and banged her arm, which is
slightly pink and swollen. e child is happy and playing
• Specic chemicals:
• beryllium.
• Drugs:
• hepatic granulomatous due to allopurinol, phenylbutazone, sulphonamides.
• Unknown:
• Crohn’s disease
• sarcoidosis
• Wegener’s granulomatosis.
with her arm in a sling, with normal observations and no
evidence of serious injury or infection. e patient’s mother
explains that the nurse practitioner performed an X-ray,
which showed no fracture but that she doesn’t understand
why it is red and sore if it isn’t infected or broken. She asks
if her daughter needs antibiotics.
1. Explain to this worried parent the dierence between
inammation, fractures and infection and answer her
question regarding antibiotics.
2. Explain to the examiners the stages of acute inamma-
tion and the key cells and mediators involved.
3. Explain to the examiners what factors in the presenta-
tion of a child to A&E would make you think of nonaccidental injury (NAI)?
OSCE Scenario 16.4
A 44-year-old female is brought in unwell with severe central abdominal pain radiating through to her back with
nausea and vomiting. Her amylase is 3400 U/L.
1. What is the diagnosis?
2. Five days later she has clinically deteriorated and is
hypotensive and anaemic. A CT scan has shown considerable bleeding in and around the pancreas. What is this
type of inammation called and why does it occur?
3. Do you know any common causes of pancreatitis?
OSCE Scenario 16.5
A 48-year-old man has accidently been given IV penicillin – he is known to have a severe allergy to all penicillinbased antibiotics. He is very unwell and has collapsed on
the ward, he is struggling to breathe, his arm is swollen and
he is profoundly hypotensive.
1. What type of shock does he have?
2. Explain why he is having diculty breathing and is
hypotensive.
3. How would you treat this patient?
Answers in Appendix pages 467–470
Please check your eBook at https://studentconsult.inkling.com/ for more self-assessment questions. See inside cover for
registration details.
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