Cell Pathology
MCD Year 1
Anil Chopra
Contents
MCD – Cell Pathology 1 – Cancer.............................................................................. 1
MCD – Cell Pathology 2 – Haemodynamic Disorders ............................................. 5
MCD – Cell Pathology 4 – Cell Injury ....................................................................... 9
MCD – Cellular Pathology 3 – Inflammation ......................................................... 11
MCD – Cell Pathology 5 - Autopsy & Forensic medicine ...................................... 16
MCD – Cell Pathology 1 – Cancer
Anil Chopra
Cancer is an important socioeconomic problem and a significant cause of morbidity
(problems, complications etc) and mortality (death) worldwide. Lung cancer is the
most prevalent in Europe.
1. Define the words hyperplasia and hypertrophy; give 2 examples of each.
Hyperplasia – increase in the size of an organ due to cell division i.e. more cells. e.g.
Hypertrophy - increase in the size of an organ due to increase size of cells i.e. larger
cells. e.g. muscular hypertrophy, ventricular hypertrophy.
2. Explain the difference between metaplasia and dysplasia giving two examples
of each.
Dysplasia – literally this means “disordered growth” and is limited to epithelium. It
is when individual cells lose their uniformity and architectural orientation. Mild to
moderate dysplasia may cause cells to revert back to normal; however severe
dysplasia results in carcinoma in situ. ('cancer in place', when a neoplastic lesion
transforms to one in which cells undergo essentially no maturation. The cells lose
their identity and become primitive cells again, which rapidly divide uncontrollably).
It is PREMALIGNANT.
Metaplasia - substitution of one mature cell type for another mature cell type which
is better suited to the environment. It is the result of a chronic stimulus which, when
withdrawn may, go back to normal. E.g. Smoking causes metaplasia of glandular
bronchial epithelium to squamous epithelium. It is adaptive, NOT
PREMALIGNANT.
3. Define the words tumour, metastasis, carcinogen
Tumour- swelling, originally for inflammation. All tumours have two basic
components
• 1. Proliferating neoplastic cells parenchyma.
• 2. Supportive stroma.
Neoplasm- new growth: “abnormal mass of tissue, the growth of which exceeds and
is uncoordinated with that of the normal tissues and persists in the same excessive
manner after the cessation of the stimuli which may have evoked the change”
4. List four features which distinguish benign from malignant tumours.
There are 2 types of tumour:
Benign tumours given suffix -oma to cell of origin e.g. Adenoma (epithelial
derivative) Fibroma (mesenchymal derivative)
Malignant tumours of epithelial origin are called carcinomas, of mesenchymal
origin are called sarcomas, lymphoma (lymph nodes), melanoma (skin –
melanocytes), seminoma (testicular cancer).
There are 4 main ways of distinguishing between benign and malignant tumours:
1. Differentiation and anaplasia (cells reverting back to immature form)
i.e. the extent to which the parenchymal cells resemble there normal counterparts.
 Benign tumours tend to be well differentiated.
 Malignant tumours show various levels of differentiation. (well, moderately,
poorly)
2. Rate of growth
 Benign tumours grow slowly
 Malignant tumours grow more rapidly
3. Local invasion
 Benign tumours grow as cohesive expansile masses that remain localised to
their site of origin (encapsulated).
 Malignant tumours infiltrate and destroy the surrounding tissue, poorly
demarcated (i.e. it is hard to see where their boundaries).
4. Metastasis
This is where a discontinuous/broken tumour implants at a distance from the site of
the main tumour mass. All malignant tumours can metastasise (with the 2 exceptions
of gliomas and basal cell carcinomas)
 This is a defining feature of malignancy. Approximately 30% patients present
with metastasis
 Benign tumours cannot metastasise.
Many tumour cells shed from primary
site daily yet only a few metastases are
produced. This is because the cells must
end up in favourable “soil”.
Metastasis occurs in a series of steps:
1.
2.
3.
4.
Detachment (integrins/cadherins)
Intravasation (proteases)
Extravasation (integrins/chemoattractants)
Angiogenesis (VEGF/bFGF)
Tumours can spread in 3 ways:
- Direct growth into body cavities e.g. peritoneal, pleural, pericardial,
subarachnoid, joint, ovarian carcinomas into peritoneal surface or spread of lung
carcinoma into pleural cavity
-
Lymphatic drainage into other organs. This is the most common route for
carcinomas. Regional nodes drain tumours which may contain the spread locally.
This may evoke an immune response which causes nodal hyperplasia (dividing of
cells). However; not every enlarged node in the region of a tumour contains
metastatic spread.
-
Spread in blood circulation; this is more typical of sarcomas (cancer of
connective tissue) but can occur in carcinomas if they invade nearby blood
vessels. Veins tend to be penetrated more frequently than arteries due to thickness
of walls. The liver and lungs are the most common sites due to the venous
drainage. E.g. Renal cell carcinoma (cancer of kidneys) can grow within the renal
vein to the IVC and then into the right atrium.
Staging of Cancer
This is a clinical classification known as the TNM method:
T: Primary Tumour size (T1-T4)
N: Nodal status (N0 or N1,2,3)
M: Presence of Metastasis (M0 or M1,2)
This is more useful than the grading of cancer which is done histologically and based
on the degree of differentiation and on the numbers of mitoses.
5. Define the terms necrosis, ulcer, degenerative, sublethal injury
Necrosis is untentional cell death, usually done by cells of the immune system.
An ulcer is an open sore of the skin, eyes or mucous membrane, often caused, but not
exclusively, by an initial abrasion and generally maintained by an inflammation, an
infection, and medical conditions which impede healing.
A degenerative disease is one which causes steady damage over time.
A sublethal injury is one which is not lethal (death causing).
6. Give two examples each of diseases caused by infection and one example of a
disease caused by a chemical agent.
RISK FACTORS/ OF CANCER

Environmental agents: UV light, occupational agents, diet and weight, alcohol,
smoking, infections notably viruses (HPV).
Carcinogens – 3 types
1. Chemicals - Some chemicals are inducers (permanent DNA damage) others
are promoters (reversible DNA damage). Neither step alone is sufficient to
cause cancer.
2. Radiation - Ultraviolet (SCC, BCC, MM) Ionising electromagnetic i.e. Xrays.
These can cause an increase in leukaemia and solid tumours.
3. Microbial agents (mainly viruses) – DNA oncogenic viruses (EBV), RNA
viruses, bacteria – helicobacter pylori.

Genetic factors: there are hereditary predispositions to some cancers. Inheritance
of a single mutant gene greatly increases the risk of developing cancer. e.g.
• lung cancer mortality four times higher in non-smoking relatives of lung
cancer patients
• inherited retinoblastoma carriers have a 10,000 fold increased risk of
developing retinoblastoma (usually bilateral)
• patiets with the gene Familial adenomatous polyposis (FAP) are 100% likely
to get colonic carcinoma by age 50.
Molecular basis Of Cancer
Cancer is caused by many genetic mutations:
There are 4 main types of gene that can have mutations leading to cancer:
1. Growth promoting genes
Oncogenes- Derived from proto-oncogenes, genes regulating normal cellular growth.
2. Growth inhibiting (tumour suppressor)
Anti-oncogenes - genes usually suppress normal cell growth. E.g. p53 (chromosome
17) 50% of all human tumours contain mutations in this gene. It prevents genetically
damaged cells from replicating.
3. Genes regulating programmed cell death
Apoptosis - bcl-2 prevents programmed cell death. Overexpression of bcl-2 and
prevention of apoptosis results in indolent growth of lymphocytes.
4. DNA repair genes
MCD – Cell Pathology 2 – Haemodynamic Disorders
Anil Chopra
In the human body, most of the water is contained in cells
(intracellular), some around the cells (interstitial) and in the
blood (plasma).
1. Describe the causes and consequences of oedema at
different sites.
Oedema is the abnormal collection of fluid within the
interstitial space. It has various causes:
• Raised hydrostatic pressure
• Reduced plasma osmotic pressure
• Lymphatic obstruction
• Sodium retention
• Inflammation
The complications include
- Cellulitis (inflammation of connective tissue beneath skin)
- Venous eczema (stasis of blood in leg leading to varicose veins)
- Venous ulcer
- Lipodermatosclerosis (condition that affects the skin just above the ankle in
patients with long-standing venous disease)
- Pulmonary Oedema (fluid accumulation in the lungs)
- Cerebral oedema (fluid accumulation in the brain)
Both hyperaemia (an active increase in blood volume, usually a regulatory response
caused by vasodilation) and congestion (passive accumulation of blood, usually from
impaired drainage) can lead to oedema.
Chronic congestion can be as a result of stasis (blood not moving) in the veins, and
as a result can lead to hypoxia (impaired
oxygenation of tissues) and as a result, tissue
damage and scarring. E.g.
Right Sided Heart Failure
Causes:
- Left sided heart failure
- Lung disease
- Valvular disease
- Congenital heart disease
Consequences: Congestion in liver, gut, spleen and
dependent subcutaneous tissues.
Left Sided Heart Failure
Causes - Myocardial disease
- Valvular disease
- Hypertension
Consequences: Congestion: pulmonary oedema and
right heart failure.
2. Define thrombosis and give the causes and potential consequences of such an
event.
Normal homeostasis maintains blood as a fluid in vessels and increases at sites of
vascular injury.
Thrombosis is a blood clot that forms, eventually blocking a blood vessel. This can
be as a result of:
• Endothelial Injury (these are all interlinked)
– Atheromatous plaques
– Myocardial infarction
– Vasculitis
– Cigarette smoke
– Hypercholesterolaemia
• Abnormal Blood flow
– Turbulence
– Stasis
• Hypercoagulability
– Primary (genetic)
– Secondary (acquired)
Other risk factors include oral contraceptive pill, malignant tumours, smoking,
pregnancy.
Thrombosis can occur in arteries, veins, endocardium and heart valves.
3. Define embolism and know about the importance of pulmonary embolism in
clinical practice.
As thromboses get particularly large, parts of them can break off forming emboli (an
embolism) which can attach itself somewhere else distant from its point of origin.
Emboli can also be fat, air, nitrogen, tumours and other foreign bodies.
If emboli attach themselves in other vessels, they can block blood flow through that
vessel resulting in ischaemia and infarction. A common place for them to be lodged
if they are anywhere in the venous circulation or in the right side of the heart, is the
vessels in the lung resulting in a pulmonary embolism:
• 2% fatal
• Most are silent
• If they are medium sized  haemorrhage/infarction
• If there is more than 60% occlusion of pulmonary vessels  sudden death
(cor pulmonale)
• There may be more than one embolism.
If the embolism is in the arterial circulation or in the left side of the heart, it can result
in emboli in:
• Brain, gut, spleen, kidney, extremities.
4. Describe possible causes of haemorrhage and potential outcomes
Haemorrhage
Haemorrhage is the leakage of blood out of a vessel due to rupture. Capillary bleeding
can lead to chronic congestion whereas venous/arterial bleeding can result in vascular
injury. It can occur externally or enclosed in tissue.
Haemorrhagic diathesis is a disorder of blood coagulation resulting in sensitivity to
bleeding.
Associated with:
Petechiae – small 1-2mm red dots on the skin and tongue where there has been
locally raised pressure as a result of minor haemorrhages.
Subcutaneous haematoma – bruising as a result of vascular fragility.
Aortic aneurysm – a swelling in the wall of the aorta which can rupture causing
serious haemorrhage.
Consequences of Haemorrhage
• Chronic anaemia (low haemoglobin)
• Hypovolaemic shock
• Low blood pressure.
5. Define shock and identify the possible causes and mechanisms.
Shock is a serious medical condition where the tissue perfusion is insufficient to meet
demand for oxygen and nutrients.
There are various causes:
- Cardiovascular collapse -> hypotension, impaired tissue perfusion, cellular hypoxia
- Severe haemorrhage
- Massive trauma
- Burns
- Myocardial infarction
- Massive pulmonary embolism
- Sepsis
There are different types of shock:
• Cardiogenic: pump failure
– Myocardial damage
– Tamponade (fluid accumulation in the pericardium)
– Pulmonary embolism
• Hypovolaemic: loss of blood/plasma
•
•
•
Septic: systemic microbial infection
Anaphylactic: hypersensitivity
Neurogenic: spinal trauma
There are also different phases to shock.
• Non progressive phase
– Reflex compensation
– Tachycardia
– Peripheral vasoconstriction
– Renal fluid retention
Patient will be hypotensive, cool, clammy, tachycardic.
•
Progressive phase
– Tissue hypoperfusion
– Circulatory/metabolic imbalance
– Acidosis
Patient will have cerebral disturbance, low urine output.
•
Irreversible phase
– Severe celluar/tissue injury
– Survival is impossible.
The various consequences of shock are:
• Brain: ischaemic encephalopathy
• Heart: subendocardial ischaemia/necrosis
• Kidneys: acute tubular necrosis
• GI tract: haemorrhagic enteropathy
• Lungs: ARDS (acute respiratory distress syndrome)
6. Define infarction and describe possible causes.
Infarction
Infarction is areas of ischaemic (caused by insufficient oxygen to tissues) necrosis
(tissue death) and is a common cause of morbidity and mortality. They cause 50% of
death due to cardiovascular disease, and 99% are caused by thrombosis or embolism.
Conditions include:
• myocardial infarction
• stroke
• venous thrombosis
• torsion (twisting of blood supply to testis)
There are 2 types of infarction:
White infarction: this is the occlusion of the end of an artery resulting in limited
blood flow to particular tissue. It is white because haemorrhage is limited to that
particular area.
Red infarction: this is venous occlusion. It is red because of the infiltration of blood
from collateral vessels into the necrotic area.
Development of an infarct can depend on nature of the vascular supply, rate of
occlusion development, vulnerability of the tissue to hypoxia and the oxygen content
of the blood.
MCD – Cell Pathology 4 – Cell Injury
Anil Chopra
1. List the causes of cell injury
Causes of cell injury:
1. Oxygen deprivation
2. Chemical agents
3. Infectious agents
4. Immunological reactions
5. Genetic defects
6. Nutritional imbalances
7. Physical agents
8. Aging
2. List the mechanisms of cell injury.
The cellular response to damaging stimuli depends on:
 the type of injury,
 its duration
 its severity
The consequences of an injurious stimulus depend on the cell’s:
 type
 status,
 adaptability
 genetic makeup
There are 4 main intercellular systems that are affected:
1. cell membrane integrity,
2. ATP generation,
3. protein synthesis and
4. the integrity of the genetic apparatus
These systems are all interlinked so that a defect in one system results in a defect in
others.
3. Define (and give examples of) hyperplasia, hypertrophy, atrophy, metaplasia and
dysplasia.
Effects of Cell Injury
Atrophy – shrinkage of cell size.
Hypertrophy – increase in cell size and usually increased organ size as a result. It is
caused by increased functional demand or hormone stimulus.
Hyperplasia – increase in the number of cells. This is caused by increase in growth
factor or other hormone stimulation.
Metaplasia – change in the cell type, i.e. replacement of one cell type with another
that is reversible.
Dysplasia – abnormal cells. This is usually when cells do not differentiate properly
and just stay immature. They are mainly precancerous cells which show the genetic
and cytological features or malignancy but not invading the underlying tissue.
4. Describe the morphological changes associated with reversible and irreversible
injury.
Changes Associated With Cell Injury
1.
Coagulative necrosis - is typically seen in hypoxic environments (e.g.
myocardial infarction, infarct of the spleen). Cell outlines remain after cell death.
2.
Liquefactive necrosis - usually associated with cellular destruction and pus
formation (e.g. pneumonia). Ischaemi in the brain produces liquefactive rather
than coagulative necrosis.
3.
Caseous necrosis - a specific form of coagulation necrosis typically caused by
mycobacteria (e.g. tuberculosis)
4.
Fat Necrosis - results from the action of lipases on fatty tissues (e.g. acute
pancreatitis, breast tissue necrosis).
5.
Apoptosis – this is cell death and has 5 main causes:
 Embryogenesis
 Deletion of auto-reactive T cells in the thymus
 Hormone-dependent physiological involution
 Cell deletion in proliferating populations
 A variety of mild injurious stimuli that cause irreparable DNA damage that
triggers cell suicide pathways
5. Describe the differences between apoptosis and necrosis.
1. Apoptosis may be physiological
2. Apoptosis is an active energy dependent process
3. Not associated with inflammation
MCD – Cellular Pathology 3 – Inflammation
Anil Chopra
1.
2.
List 4 causes of acute and 3 of chronic inflammation.
State three possible outcomes of acute inflammation due to a pyogenic microorganism.
3.
Describe briefly how the microscopic features of acute inflammation differ
from those of chronic inflammation
4.
Define the terms ‘resolution’; ‘suppuration’; ‘organisation’
5.
Describe the microscopic features of granulomatous inflammation and give 2
examples
Inflammation is the reaction of living vascularised tissue to sub-lethal cellular injury.
It occurs to remove the cause of the injury and to initiate repair of the damaged tissue.
Acute inflammation – onset and duration is hours/days.
Chronic inflammation – onset and duration can be weeks/months.
Inflammation is caused by:
• Infection.
• Foreign bodies
• Tissue destruction – mechanical trauma, chemical injury, radiation injury,
endogenous (autoimmune reaction, crystal deposition)
Acute Inflammation: This is the rapid migration of cells and mediators to the site of
injury and initiation of host defense. Stimuli can include: infection, trauma,
physiochemical, foreign body, immune reactions.
Signs of inflammation: - redness, swelling, heat and pain.
Systemic features: - fever shock.
Vascular Changes
Vascular flow increased: blood vessels supplying the injured tissue dilate which is
what causes the redness and heat.
Adhesion Molecules expressed on the Endothelium: this is so that the inflammatory
cells can stick to the vessel walls.
Increase in Vascular Permeability: leaky capillaries allow cells and mediators to
enter tissue as fibrin exudes from the tissues. This is what causes swelling.
White cell Changes
White blood cells leave the blood and enter the injured tissue to become activated:
Neutrophils are recruited: these are granulated cells, produced in the bone marrow
which phagocytose debris, bacteria and foreign bodies by release the contents of their
granules (enzymes, free radicals and soluble mediators).
 Oxygen dependent Cell Killing: Formation of highly reactive oxygen
containing compounds with unpaired electrons which make chemical bonds
readily with anything to hand, disrupting normal bacterial molecules.
 Oxygen independent cell killing: this mainly involves enzymes e.g.
o Bactericidal permeability increasing protein – “does what is says on
the tin” - causes phospholipid degradation
o Lysozyme - Enzyme degrades bacterial glycoprotein coat
o Lactoferrin - binds iron, important element in bacterial biochemistry
o Major basic protein - cytotoxic to many parasites
o Defensins - cytotoxic to microbes
o Other enzymes - e.g. elastases
Macrophages are also recruited: these are Monocytes in the blood and specialise into
tissue macrophages as they enter different systems. They also phagocytose as well as
controlling other inflammatory cells by the release of cytokines. This is results in
chemotaxis:
 Chemotaxis is locomotion orientated along a chemical gradient. Exogenous
(bacterial products) and endogenous compounds (complement, cytokines,
leukotrienes) attract cells. Surface receptors bind to these products and so
recognise the chemical gradient. They then mediate changes in cytoskeleton polymerising and reorganising actin.
The inflammatory cells and the exudates together form pus. The exudates include
fluid and the fibrin.
Other changes in the process of inflammation include:
- activation of the complement system
- clotting factors and platelet activation factors
- tumour necrosis factors (TNF and IL)
Outcome of Inflammation
1) Resolution – i.e. tissue returns back to normal. This only occurs if the tissue
contains cells that can regenerate those cells that were lost, and if the
extracellular matrix is still intact.
2) Abscess – occur if organisms are immunosuppressed. This is a collection of
pus that has accumulated in a cavity formed by the tissue.
Chronic Inflammation
Chronic inflammation is: inflammation of prolonged duration in which active
inflammation, tissue destruction and attempts at repair occur simultaneously. It is
caused by:
• Persistent damage
– Persistent infection
– Prolonged exposure to toxic agent
•
•
•
– Autoimmunity
Significant damage
Key cells are different
– Macrophages
– Lymphocytes
• B cells
• T cells
– Eosinophils -Seen in allergic and parasitic causes of inflammation
– Mast cells - seen in allergic diseases
– NO exudate
Special types
– Granulomatous – a granuloma is a collection of macrophages caused
by infections, foreign material and reactions to tumours.
Consequences of Inflammation
•
•
•
•
•
•
•
•
•
6.
Fever
Acute phase proteins - produced by liver
– C reactive protein - CRP
– Serum amyloid A protein - SAA
– Fibrinogen (increases erythrocyte sedimentation rate)
Anorexia, malaise (faintness, uncomfort)
Shock (severe inflammatory reaction, e.g. sepsis)
Oedema (swelling) e.g. laryngeal
Tissue Damage
Scarring
Weight loss (cachexia)
Protein loss
Name two local, and two general, causes for a failure of healing or repair.
Defective inflammation results in improper healing and as a result, increases
susceptibility to infection. This can have various causes:
• POOR NUTRITION - Protein needed for collagen tensile strength
• VITAMIN DEFICIENCY
– Vitamin C – needed by fibroblasts to make collagen
– Vitamin A - required for epithelium
• MINERAL DEFICIENCY
– E.G. ZINC
• SUPPRESSED INFLAMMATION
– E.G. By Steroids
– Old age
– Diabetes
• POOR BLOOD SUPPLY
• PERSISTENT FOREIGN BODY
• MOVEMENT
MCD – Cell Pathology 5 - Autopsy & Forensic medicine
Anil Chopra
1. Explain how the need for consent from the deceased’s’ relatives differs for a
Coroners’ and a Hospital Autopsy.
There are Two types of Autopsy
1. Hospital
Consent must be obtained from the relatives
With the relevant consent, any material can be taken
2. Coroners
No consent of family needed (but their wishes should be considered)
Material can only be taken if it bears upon the cause of death (with Coroner’s
permission)
2. List four types of death that must be reported to the Coroner.
Who is the Coroner?
An independent judicial officer of the crown who has a statutory duty to investigate
the circumstance of certain categories of death for the protection of the public.
Cases that must be reported to the Coroner
• The cause of death is unknown
• The deceased has not been seen by the certifying doctor either after death or
within the 14 days before death
• The death was violent, unnatural or suspicious
• The death may be due to an accident (whenever it occurred)
• The death may be due to neglect by self or others
• The death may be due to an industrial disease or due to the deceased persons
employment
• The death may be due to an abortion
• The death occurred during an operation or before recovery from the effects of an
anaesthetic
• The death may be a suicide
• The death occurred during or shortly after detention in police or prison custody
• The death may be related to poisoning
• If in any doubt the case must be discussed with the Coroner’s office.
Coroners autopsy
Conducted to establish the cause of death
Once Coroner has the cause of death his remit is over
3. List two reasons for conducting Hospital Autopsies.
Reasons for hospital autopsy
Allows a very thorough examination of the deceased, the extent of their disease, their
treatment and its effects
For:
– Audit – Major discrepancies between stated cause of death and actual cause of
death (main diagnosis missed in 15% of cases subsequently autopsied)
– Monitoring effectiveness of new treatments e.g. complex congenital heart disease.
– Teaching e.g. unrivalled clinic pathological correlation.
– Research e.g. knowledge of variant CJD relies heavily on study of post mortem
brain tissue.
So What?
Death certificate data used for epidemiology
i.e. Accurate morbidity and mortality data is needed to monitor the nations health, to
direct the allocation of scanty resources and to detect environmental risks.
The Death Certificates
Filled in for any death
Taken to Registrar (of Births, Deaths & Marriages) by family
Scrutinised and must be correct before registration of death possible
1a Immediate cause of death (must be filled in)
1b Predisposing factor
1c Predisposing factor
2 Other factors contributing to but not directly leading to death
E.G. – 1a Gun shot wound to head
or
1a Haemopericardium
1b Myocardial infarction
1c Ischaemic heart disease
2 Hypertension
4. List four causes of sudden unexpected death in the community.
Natural causes of sudden unexpected death (in the community)
Cardiovascular disease
 Coronary artery disease
 75% (approximately) of deaths handled by medical examiners in USA
 50% die suddenly
 25% die without any preceding history or warning
 Cardiac Arrhythmia is usual mode of death
 Severe coronary artery atherosclerosis is most common anatomical finding
 Usually in 2 or more major vessels
 Usually 75% or greater stenosis to cause death
 Other findings include:
o Myocardial scarring
o Coronary artery thrombosis
o Acute or subacute MI (myocardial infarction)
 If arrhythmia is the mechanism of death the diagnosis is one of exclusion, full
autopsy must be conducted and severe coronary atherosclerosis must be the major
finding.
 (In such cases cause of death usually stated as1a Ischaemic heart disease)
Hypertensive heart disease
Usually accompanied by coronary artery atherosclerosis
 Cardiomegaly with symmetrical left ventricular hypertrophy
 Acute cardiac arrhythmia is usual cause of death
 Other Cardiac Causes of Sudden Unexpected Death
 Cardiomyopathy
 Myocarditis
 Structural anomalies (e.g. bridging)
 Floppy mitral valve
 Aortic stenosis (usually calcific)
 Conduction abnormalities (e.g. long QT syndrome)
 Vascular System
 Ruptured aortic aneurysm associated with atherosclerosis & hypertension
Central Nervous System
 Non traumatic subarachnoid haemorrhage:
 (Usually due to Berry aneurisms, 2-4% adults, 90% silent until rupture 2/3
symptomatic
 between 40 & 65 years old)
 Intracerebral haemorrhage:
 10-30% of all strokes most common cause is hypertension.
 Epilepsy
Respiratory System
 Pulmonary embolus
 Asthma
Gastro Intestinal Tract
(Not usually unexpected or sudden)
 Bleeding Oesophageal Varices
 Bleeding Ulcers
 Pancreatitis
Other Causes of Sudden Unexpected Death (in the community)- (Not Natural)
DRUGS
Alcohol
 Not usually a cause of sudden unexpected death (but can be in alcoholics).
 Often associated with GI problems.
 Often alcohol related damage goes with drug use so think of drugs when you see it.
TRAUMA
 Self induced
 Caused by others
5. What is a bruise? Give an example of a mechanism of injury that would lead to a
bruise.
What is a Bruise Or contusion
A blunt trauma injury. Occurs alone (skin intact) or is associated with other injuries.
An extraversated collection of blood which has leaked from damaged small arteries,
venules and veins but not capillaries Occur more easily where skin is lax. Fragility of
vessels, coagulation state etc all effect bruising. May take hours or days to form. May
get patterned bruises (can see better with special light sources). Deep bruising may
never be seen on the surface. You can bruise after death (but usually small and lie on
dependant parts). Not everything is a bruise: e.g. Pink areas may be due to
hypothermia.
6. What is an abrasion? Give an example of a mechanism of injury that would lead
to an abrasion.
What is an abrasion ?
A graze or scratch. The most superficial of blunt trauma injuries.
Confined to the epidermis (strict definition) but may actually extend into the
superficial dermis due to skin anatomy). Can occur before and after death. Due
tangential force – may have a distal skin tag eg Friction burn, or Vertical force eg
Stamp – no distal skin tag. Abrasion examples - Friction burn, Car radiator, Flooring,
Whip, Stamp.
7. What is a laceration? Give an example of a mechanism of injury that would lead
to a laceration.
Laceration
A split to the skin. The result of blunt force overstretching the skin. Usually pass
through the full thickness of the skin. They are deep and will bleed. Margins ragged
with crushing and bruising. “Bridging fibres” arch across the skin defect. Common
where skin can be compressed between the force and underlying bone e.g. Scalp,
elbow, shin. Rare over soft fleshy areas e.g. Buttocks, breasts. A laceration shows
poor reproduction of the object causing it. “Flaying” – tangentially applied force
leading to a horizontal laceration. examples – Fall, Punch, Stick, Hammer, Bomb,
Wheel of car (flaying).
8. What is the difference between a cut and a stab? Other than a knife, what might
cause such a wound?
Cut & Stab wounds
Cut (or slash)
The length of the injury is longer than its depth Stab(or penetrating injury). The depth
of the wound is greater than the width
Cut & Stab Wounds
Causes by an object with a sharp or cutting edge. Usually a knife but can be anything
eg a broken glass or bottle or a piece of metal. Edges are clean and well demarcated.
Minimal injury to surrounding tissue. Information about weapon type can be gained
from the wound but beware of over interpretation.
N.B “Incised Wounds”
Some discrepancy in terms used (Knight). To some (e.g. Rutty/Burton) includes cuts
& stabs. To others (e.g. Shepherd) is synonymous just with cuts.
9. What is the best generic term to use when describing physical damage to a
patient?
When describing wounds either use the correct term or use a generic term
such as INJURY.