Pathological processes
E. Herbert
Manifestation
of damage to
tissue cells
 Necrosis
 Def: Death of tissue cells within localised area
 Cause: Tissue damage because of lack of oxygen
(Hypoxia) or too little oxygen reaching the tissue
(anoxia)
 Necrosis followed by putrefactive process results in
gangrene
Gangrene
 Dry gangrene: arterial occlusion e.g. diabetic foot
 Moist gangrene: Obstruction of blood to intestines
Dry gangrene affecting the toes as a result of peripheral artery
disease
Gangrene
 Gas gangrene
 Cause: Clostridia bacteria
 Destruction of tissue
resulting in formation of
gas.
 Infection spreads fast
 Results in toxemia
Degeneration
 Damage causing structural changes to
tissue cells.
 Fatty degeneration
 Accumulation of fat in specialized cells
of organs e.g. heart or liver
 Causes: hypoxia, diabetic
insufficiencies, alcoholism, severe
infections
 Abnormal deposits of
calcium salts in soft tissue
of body
Pathological
calcifications
 Dystrophic pathological
calcification: calcium salts
deposited in cells-killed or
injured e.g. healed TB
Renal TB calcifications
Lungs
There are numerous, punctate calcifications in the spleen and
calcification in
two mesenteric lymph nodes.
 Any process with elevated
calcium phosphate levels
Metastatic
calcification
 Calcium deposits in
previously healthy tissue
caused by another
pathological calcification,
e.g. hyperparathyroidism,
renal failure, sarcoidosis
 Calcification formed in
small veins.
 Commonly found in pelvis
Phleboliths
Literally "vein stones",
and represent
calcification within
venous structures.
They are particularly
common in the pelvis
where they may mimic
ureteric calculi, and
are also encountered
frequently in venous
malformations
Brain
calcifications
 Too much calcium or phosphorus in the blood.
 Inflammation or damage to the site
Brain
calcifications
Infection
 Infection caused by
pathogenic microorganisms
 Types of germs
 Infection results in tissue
damage.
 Viruses: e.g. herpes virus,
measles
 No symptoms = subclinical
infection (healthy carrier)
 Fungi: ringworm
 Bacteria: e.g. cocci, bacilli,
spirochaetes
 Protozoa: malaria
Spread of
infection
 Inhalation: via respiratory
tract
 Ingestion: swallowed
 Inoculation: wounds /
penetration of undamaged
skin
 Orifices, anus, vagina,
urethra
 Clinical signs & symptoms:
 Site: swelling, redness,
heat & pain
 General: pyrexia (fever),
headache, anorexia,
malaise
Defence
mechanisms
 Surface defence: skin &
mucous membranes
 Internal defence:
 Antibodies
 Phagocytosis
 Presence of complement
(chemical agent)
 Inflammatory reaction
enables concentration of
antibodies, phagocytes &
immune cells at site of
infection
Immunity
 Acquired internal defence
mechanism producing
specific antibodies or
specific immune cells
against pathogens
 Harmful immune
responses e.g. tissue
rejection when receiving a
transplant
 Passive immunization
 Adaptive or Active
immunization:
 Long-lasting protection
Immunization
 Vaccine per injection,
mouth, scarification of
skin, or multiple pressure
technique
 Vaccines consist of living
pathogens, dead
pathogens or modified
toxoids (tetanus)
 Short-lived protectionantibodies can be removed
from the host and
transferred into another
recipient where they
provide immediate
immunity
 E.g. epidemic of infective
disease
Defective
immune response
 AIDS:
 Virus cause defective
cellular immunity
 Complications: Kaposi’s
sarcoma & Pneumocystis
carinii pneumonia
 Immune suppressive
therapy: to prevent tissue
rejection
 Local reaction of body to damage of cells
Inflammation
 Infection cause of inflammation
 Inflam. reaction produces inflam. exudate = blood
cells, plasma & antibodies.
1. Acute Inflammation
Resolution:
Minimal tissue
damage
Return to normal
Sequela of
inflammatory
reaction
Suppurative:
Pus forms cavity
known as abscess
Ruptured abscess
Cause: sinus tract
fistula
Ulcer:
Open sore on skin
from inflam. process
Repair & organisation
Excess of exudate
Or necrosis
Fibrosis:
Fibrous adhesions
forms
between tissues
2. Chronic Inflammation:
Result if causative factor not removed
Spread of
infection
 Lymphangitis: inflammation of
lymph vessels
 Pyaemia: multiple secondary
abscesses
 Lymphadenitis inflammation of
lymph glands
 Septicaemia: presence of
multiplying pyogenic microorganisms in bloodstream →
 Metastatic infection: spread via
blood
 Empyaemia: collection of pus in
hollow organ
- clinical signs; fever, pallor,
hypotension
 Gliosis: repair of neuroglia
 Repair is effort by body to
restore continuity in tissue
Repair
 Regeneration: repair by
multiplication of undamaged
specialized cells
 Fibrosis: repair by: granulation
tissue converted into fibrous
connective tissue resulting in
avascular scar tissue
 Complications:
 Scar tissue in hollow structure
can cause stricture / stenosis
 Fibrosis in cavities can cause
bands of adhesions
 Keloids: Production of tumourlike scars
Plain films
 Soft-tissue swelling
 Inflammatory exudate e.g.
pneumonia
 Abscess formation e.g.
lung abscess
How Co19 appears on x-rays
Pneumonia
 Atrophy : shrinkage in size of
organs or tissues
 Hypertrophy: increase in
size of individual cells. Can
be physiological
Disorders of
growth
 Hyperplasia: increased celldivision
 Agenesis: congenital
absence
 Hypoplasia: defective
development of normal
size
 Dysplasia : disordered cell
growth/ abn cells in tissue
 Metaplasia: change in tissue cell
from one type to another
 Anaplasia: Mature cells returning
to primitive type: normal malignant
Drug induced gingival Hyperplasis
Ectopic kidney
Disorders of
growth
Horseshoe
kidney
Lower poles of kidney is connected
 Means new growth:
formation of neoplasms or
tumours
 Benign:
 slow growth
 displaces normal tissue
Neoplasia
 Malignant:
 Rapid growth
 Infiltrate surrounding
tissue
 Serious general effects in
body
 harmless but can be fatal if
 Fatal if untreated
causing pressure on
important organs
 Distant spread, forming
metastases
 Encapsulated
 No distant spread
Nephroblastoma
vs Neuroblastoma?
The development of secondary malignant growths at a distance
from a primary site of cancer.
Metastasis
Neoplasia
 Carcinomas: spread via
lymphatics & blood
 Anaplastic: absent
similarity to original cells
 Sarcomas: spread only via
blood
 Carcinogens: cancerproducing agents
 Differentiated neoplasms:
cells show similarity to
original cells
 Carcinoma-in-situ:
localized growth – inside a
specific area (no spread)
Tech Tip
 Cancers of epithelial tissue such as adenocarcinoma
are additive in nature and require increased kVp.
Many bone cancers, such as osteosarcoma, will
deplete the bone cells and are considered
destructive. These require a decrease in kVp.
 Abnormal cavities containing fluid or semi-fluid
material, or air:
 Possess lining material
Cyst formation
 Causes:
 Congenital
 Trauma
 Infection
 Obstruction of glandular ducts
 Neoplastic
Complication
of cyst
Disorders in
blood
circulation
 Haemorrhage: bleeding;
trauma or disease
 Haematuria: blood in urine
 Epistaxis: nose bleed
 Antepartum haemorrhage:
bleeding from pregnant
uterus
 Haematemesis: vomiting
of blood
 Haemoptysis: coughing up
of blood
 Melaena: blood in stools
 Hyperaemia
 Congestion: excess blood in
part or parts of body
Disorders in
blood
circulation
 Local Hyperaemia:
inflammation / obstruction
of veins
 General venous congestion:
R-side HF; RV ↓ →
↑pulmonary circulation
 Oligaemia: reduction in
blood present; PA stenosis
 Anaemia: ↓ Haemoglobin /
↓ number of red cells
 Ischaemia
 (local anaemia): e.g.
ischaemic heart disease
 Thrombosis: formation of
blood clot
Disorders in
blood
circulation
 Phleboliths: calcified
thrombi in veins
 Embolism: detached
thrombus carried via blood
to another part of body
 Infarct: Impaction of
embolus; causes ↓ blood
supply; area of dead tissue
 Oedema: excessive fluid in
tissue spaces; fluid
contains blood plasma;
causes: venous
obstruction; HF, Kidney
failure
 Ascites: oedema of
peritoneal cavity
 Pleural effusion: oedema in
pleural cavity
Pulmonary
oedema
 Many causes
 Unilateral / bilateral
 ↑Fluid in alveolar walls
 ↑Fluid in alveolar spaces
Disorders in
blood
circulation
Pleural effusion
Ascites
Acute
circulatory
failure (shock)
 Deficient oxygenation of
tissue cells
 Septicaemic: severe
infections
 Types of shock:
 Clinical signs:
 Hypovolaemic: ↓blood
volume/ extracellular fluid
 Giddiness
 Cardiogenic: ↓ cardiac
output; heart suddenly can't
pump enough blood to meet
your body's needs
 Neurogenic: circulatory
disturbance from nervous
cause
 Pallor
 Coldness
 Anxiety
 Fainting
 Rapid pulse
 Hypotension
Hypersensitivity
& allergy
 Abnormal reaction by body
to certain foreign materials
 Variety of agents can
provoke allergic reactions
 E.g. asthma, hay fever,
eczema, food allergy,
certain drugs
 Acute rheumatism & acute
glomerulonephritis–
allergic reaction to
streptococcal infection
 Anaphylactic shock: acute
allergic reaction;
circulatory collapse; can be
fatal
 Treatment: antihistamines
 Allergic reaction to contrast media: urticaria
(nettlerash), swelling of eyelids & soft tissues of face &
neck, dyspnoea
Hypersensitivity
& allergy
 Certain substances in tissues develop antigenic
properties, causing formation of auto-antibodies.
 Results in antigen-antibody reaction
Autoimmunity
 Causes diseases termed as autoimmune disease e.g.
RA, Hashimoto’s thyroiditis
 Blood test determine autoimmune profile (different
kinds of auto-antibodies in blood)
Homework:
 Describe the wound healing process.