flashcards
1
Q
What is aetiology?
A
Aetiology is the cause of a disease, which can be genetic, environmental, or multifactorial.
2
Q
What is pathogenesis?
A
Pathogenesis refers to the mechanisms through which aetiology operates to produce pathological and clinical manifestations of a disease.
3
Q
What are the three main categories of aetiology?
A
Genetic, environmental, and multifactorial.
4
Q
What is an idiopathic disease?
A
A disease with an unknown cause.
5
Q
What is a risk factor in disease?
A
A condition or behaviour associated with an increased likelihood of developing a disease.
6
Q
Name three mechanisms of pathogenesis.
A
Inflammation, degeneration, carcinogenesis.
7
Q
What is inflammation?
A
A response to harmful agents causing tissue injury.
8
Q
What is degeneration?
A
The deterioration of cells or tissues due to failure of adaptation.
9
Q
What is carcinogenesis?
A
The process by which cancer-causing agents lead to tumour formation.
10
Q
What is the difference between a symptom and a sign?
A
A symptom is what the patient experiences (e.g., pain), whereas a sign is what a doctor observes (e.g., high blood pressure).
11
Q
Give an example of a specific symptom.
A
Diarrhoea or a skin rash.
12
Q
What is a syndrome?
A
A combination of signs and symptoms characteristic of a particular disease.
13
Q
What are some symptoms of Cushing’s syndrome?
A
Obesity, hypertension, thinning skin, and reddish-purple stretch marks.
14
Q
What is a lesion in pathology?
A
A structural or functional abnormality responsible for ill health.
15
Q
What is a disease complication?
A
A secondary or prolonged effect of a disease.
16
Q
What is an example of a disease complication?
A
A lung embolism resulting from thrombosis in the leg.
17
Q
What is prognosis?
A
The anticipated outcome of a disease.
18
Q
What factors influence prognosis?
A
Medical or surgical intervention and disease severity.
19
Q
Define morbidity.
A
The incidence or prevalence of illness in a population.
20
Q
What is mortality in epidemiology?
A
The probability of death as the outcome of a disease.
21
Q
Define prevalence.
A
The total number of cases of a disease in a specified population at a given time.
22
Q
How is prevalence different from incidence?
A
Incidence refers to new cases, while prevalence includes all existing cases.
23
Q
What is a transcriptional activator?
A
A protein that increases gene expression by binding to a promoter or enhancer.
24
Q
How can a gene be regulated by moving it to a different location?
A
It can be placed under the control of a different promoter, altering when and where it is expressed.
25
What is epigenetics?
The study of heritable changes in gene expression without changes in DNA sequence.
26
Name one mechanism of epigenetic regulation.
DNA methylation.
27
What is alternative splicing?
A process where different exons are joined together to create multiple mRNA variants from a single gene.
28
What is polyadenylation?
The addition of a poly(A) tail to mRNA to stabilise it.
29
Name the three stages of translation.
Initiation, elongation, and termination.
30
What happens during translation initiation?
The ribosome assembles around the start codon.
31
What is the role of chaperone proteins in translation?
They assist in proper protein folding.
32
What is aetiology?
Aetiology is the study of the causes of diseases. It includes genetic, environmental, and multifactorial causes.
33
What is pathogenesis?
Pathogenesis refers to the biological mechanisms by which an aetiological factor leads to the structural and functional changes seen in a disease.
34
What are the key differences between aetiology and pathogenesis?
- Aetiology identifies the cause of a disease.
* Pathogenesis explains how the cause leads to the development of the disease.
35
What are the different types of aetiological factors?
* Genetic: Inherited mutations or disorders acquired during conception.
* Environmental: Includes infections (bacteria, viruses, fungi, parasites), chemical exposure, and physical trauma.
* Multifactorial: A combination of genetic predisposition and environmental influences.
36
What does 'idiopathic' mean in medicine?
It refers to diseases with no known cause.
37
What is a risk factor?
A condition or behaviour that increases the likelihood of developing a disease, such as smoking for lung cancer.
38
What are the main mechanisms of pathogenesis?
1. Inflammation: The immune response to infection or injury.
2. Degeneration: The deterioration of cells due to ageing, toxins, or metabolic issues.
3. Carcinogenesis: The transformation of normal cells into cancerous cells due to genetic mutations and environmental triggers.
39
How does inflammation contribute to disease?
Inflammation helps eliminate harmful stimuli but can cause tissue damage if prolonged (chronic inflammation).
40
What is the role of degeneration in disease?
It leads to loss of function in tissues or organs, as seen in neurodegenerative diseases.
41
What is carcinogenesis?
The process by which normal cells acquire mutations that result in uncontrolled cell growth, forming tumours.
42
What is the difference between symptoms and signs?
* Symptoms: Subjective experiences reported by the patient (e.g., fatigue, pain).
* Signs: Objective measurements observed by a healthcare professional (e.g., fever, high blood pressure).
43
What is a syndrome?
A collection of symptoms and signs that together indicate a specific disease or disorder.
44
What are examples of specific symptoms?
* Diarrhoea (indicative of gastrointestinal issues).
* Skin rash (possible allergic reaction or infection).
45
What are the key clinical features of Cushing’s syndrome?
* Obesity.
* Hypertension.
* Thinning skin that bruises easily.
* Reddish-purple stretch marks on the abdomen and thighs.
46
What is a lesion in pathology?
A lesion is a structural or functional abnormality that is the direct cause of disease symptoms, such as an infarct in a heart attack.
47
What is a complication of disease?
A secondary effect that arises due to the primary disease. For example, a pulmonary embolism can occur due to a deep vein thrombosis.
48
What is prognosis?
Prognosis is the expected outcome of a disease, influenced by factors such as severity, treatment, and patient condition.
49
What is an example of prognosis in lung cancer?
The 5-year survival rate for lung cancer is approximately 5%.
50
What is morbidity?
The incidence or prevalence of illness in a population.
51
What is mortality?
The likelihood that a disease will result in death, often expressed as a percentage.
52
What is prevalence?
The total number of cases of a disease in a specific population at a given time.
53
How does prevalence differ from incidence?
Incidence refers to the number of new cases within a specific timeframe, while prevalence includes all existing cases.
54
What is a transcriptional activator?
A protein that binds to DNA to enhance gene expression by promoting RNA polymerase binding.
55
How can the location of a gene affect its expression?
If a gene is moved to a different promoter, its expression may change, leading to altered timing and levels of gene activity.
56
What is epigenetics?
The study of heritable gene expression changes that do not involve alterations in the DNA sequence.
57
What are two major epigenetic mechanisms?
1. DNA methylation: Silences genes by adding methyl groups to DNA.
2. Histone modification: Alters chromatin structure to increase or decrease gene expression.
58
What is alternative splicing?
A process where different combinations of exons are joined together, allowing a single gene to produce multiple proteins.
59
What is polyadenylation?
The addition of a poly(A) tail to the 3’ end of mRNA, increasing its stability and translation efficiency.
60
What are the three stages of translation?
1. Initiation: The ribosome assembles around the start codon.
2. Elongation: Amino acids are added to the growing polypeptide chain.
3. Termination: The ribosome reaches a stop codon, and the polypeptide is released.
61
What is the role of chaperone proteins?
They assist in the proper folding of newly synthesized proteins.
62
How does translation regulation affect protein production?
It controls the efficiency of protein synthesis, impacting cellular function and adaptation to environmental changes.
63
What are the key aetiological factors for lung cancer?
* Smoking.
* Exposure to carcinogens like asbestos.
* Genetic predisposition.
64
What is the pathogenesis of lung cancer?
Chronic exposure to carcinogens leads to genetic mutations that cause uncontrolled cell division and tumour formation.
65
What is the relationship between aetiology, pathogenesis, and disease in hypertension?
* Aetiology: Genetic predisposition, obesity, high salt intake.
* Pathogenesis: Increased arterial resistance, elevated blood pressure.
* Disease: Damage to blood vessels, risk of stroke or heart attack.
66
True or False: Idiopathic diseases have an unknown cause.
True
67
True or False: Pathogenesis refers to the direct cause of disease rather than its mechanism.
False
68
True or False: Congenital diseases are always inherited from parents.
False
69
True or False: Prognosis describes the likely outcome of a disease.
True
70
True or False: Aetiology is the study of disease mechanisms.
False
71
What is diagnosis?
The process of identifying a disease in an individual through clinical history, physical examination, and laboratory investigations.
72
What is the first step in diagnosing a disease?
Documenting the patient’s symptoms.
73
What does a doctor look for during a physical examination?
Clinical signs.
74
What is a diagnostic laboratory test?
A test performed on patient samples to assess biomarkers or detect abnormalities.
75
What are the two types of diagnostic laboratory tests?
- Quantitative measurement (compared to normal reference values).
* Subjective assessment (evaluated by a pathologist).
76
What is epidemiology?
The study of disease patterns in populations and how diseases spread over time and place.
77
What are the main aims of epidemiology?
- Identifying disease causes and risk factors.
* Planning disease prevention strategies.
* Providing adequate healthcare facilities.
* Population screening for early disease detection.
78
Give an example of an epidemiological study.
Hepatitis Delta Virus (HDV) studies or age-specific prevalence of coronary heart disease in Australia.
79
What are two main study designs in epidemiology?
Prospective studies (follow subjects over time) and retrospective studies (analyse past exposures).
80
What is relative risk?
A statistical measure used in epidemiology to estimate the likelihood of disease occurrence in an exposed group compared to an unexposed group.
81
What is an autopsy?
A post-mortem examination performed to determine the cause of death and gather medical insights.
82
What are the two main types of autopsies?
Medicolegal autopsies (forensic investigations) and clinical autopsies (for medical research and education).
83
Who performs medicolegal autopsies?
Forensic pathologists.
84
What percentage of diagnostic discrepancies are revealed by autopsies?
Around 30%.
85
What is cell injury?
The response of cells to stress, which can be reversible or irreversible.
86
What are the two main outcomes of cell injury?
- Reversible injury: Cells recover.
* Irreversible injury: Leads to cell death.
87
What are the two main types of cell death?
- Necrosis (uncontrolled cell death due to injury).
* Apoptosis (programmed cell death).
88
What are the key morphological changes in reversible cell injury?
Swelling of the endoplasmic reticulum and mitochondria, followed by chromatin clumping.
89
What are the main causes of cell injury?
- Hypoxia (oxygen deprivation).
* Physical trauma (mechanical injury, extreme temperature).
* Chemical agents (cyanide, alcohol, carbon monoxide).
* Infectious agents (bacteria, viruses).
* Immunologic reactions (allergic responses).
* Nutritional imbalances (vitamin deficiencies, malnutrition).
* Genetic abnormalities (sickle cell anaemia).
90
What is hypoxia?
Reduced oxygen supply due to conditions such as ischemia or respiratory failure.
91
What is anoxia?
The complete lack of oxygen supply, leading to severe tissue damage.
92
What is ischemia?
The death of cells due to blood supply restriction, leading to a lack of oxygen and nutrients.
93
What determines the cellular response to injury?
The nature, severity, and duration of the injury.
94
What factors influence the consequences of cell injury?
The cell type, functional state, and adaptability.
95
What causes functional and biochemical abnormalities in injured cells?
Damage to essential cellular components like mitochondria, plasma membrane, DNA, and proteins.
96
What are free radicals?
Highly reactive molecules with unpaired electrons that damage cellular components.
97
How are ROS generated?
- Radiation exposure (UV light, X-rays).
* Normal metabolic reactions.
* Transition metals like iron donating electrons.
98
What are the three main types of ROS-induced cell injury?
- Lipid peroxidation (damaging membrane lipids).
* Protein oxidation (disrupting enzyme functions).
* DNA damage (mutations and strand breaks).
99
How does ROS cause DNA damage?
The reaction of ROS with thymine in nuclear and mitochondrial DNA, leading to single-strand breaks.
100
How do cells protect themselves from ROS damage?
Antioxidant enzymes such as superoxide dismutase, catalase, and glutathione peroxidase neutralise ROS.
101
What are the four main types of cellular adaptations?
- Hypertrophy (increase in cell size).
* Hyperplasia (increase in cell number).
* Atrophy (decrease in cell size and function).
* Metaplasia (change from one cell type to another).
102
What is atrophy?
A reduction in cell size and function due to reduced workload, poor nutrition, or ageing.
103
What is metaplasia?
The replacement of one cell type with another due to environmental stress.
104
What is the difference between apoptosis and necrosis?
Apoptosis is a controlled, energy-dependent process that does not trigger inflammation, whereas necrosis is an uncontrolled process that results in cell lysis and inflammation.
105
Do mitochondria regulate apoptosis?
Yes, mitochondria play a central role by releasing cytochrome c, which activates caspases in the apoptosis pathway.
106
What is the role of p53 in apoptosis?
The p53 tumour suppressor gene regulates apoptosis by inducing pro-apoptotic proteins when DNA damage is detected.
107
What are the key stages in the progression of cell injury?
Reversible injury → Irreversible injury → Cell death (necrosis).
108
What are the early functional changes in cell injury?
* Decreased ATP production
* Loss of cell membrane integrity
* Defects in protein synthesis
* Cytoskeletal damage and DNA damage
109
What are the morphological changes seen in reversible cell injury?
* Light microscopy: Cellular swelling
* Ultrastructural changes: Plasma membrane blebbing, mitochondrial swelling, dilation of the ER, nuclear alterations
110
What happens when cell injury becomes irreversible?
Extensive damage to all membranes, swelling of lysosomes and mitochondria, increased intracellular calcium, activation of catabolic enzymes, and nuclear fragmentation.
111
What are the three nuclear changes observed in irreversible cell injury?
1. Pyknosis – Nuclear shrinkage
2. Karyorrhexis – Nuclear fragmentation
3. Karyolysis – Nuclear dissolution
112
What is necrosis?
Pathological cell death in a living organism due to enzymatic degradation of lethally injured cells.
113
What are the four main types of necrosis?
1. Coagulative necrosis
2. Liquefactive necrosis
3. Caseous necrosis
4. Fat necrosis
114
What is the most common type of necrosis?
Coagulative necrosis.
115
In which tissues does coagulative necrosis typically occur?
All tissues except the brain following hypoxic injury.
116
What are the key microscopic features of coagulative necrosis?
Preservation of cell architecture with loss of nuclei and coagulated eosinophilic cytoplasm.
117
What type of necrosis is characteristic of bacterial infections and CNS hypoxic injury?
Liquefactive necrosis.
118
What causes liquefactive necrosis?
The accumulation of inflammatory cells, leading to enzymatic digestion of dead cells into a liquid mass.
119
What is the gross appearance of caseous necrosis?
A cheesy, yellow-white appearance due to tissue destruction, commonly seen in tuberculosis.
120
What disease is most commonly associated with caseous necrosis?
Tuberculosis.
121
What is fat necrosis?
A focal area of fat destruction due to pancreatic lipase release, commonly seen in acute pancreatitis.
122
What is a characteristic feature of fat necrosis?
White chalky calcium soap deposits at lipid breakdown sites.
123
What is apoptosis?
A regulated process of programmed cell death that removes unwanted or damaged cells without causing inflammation.
124
How does apoptosis differ from necrosis?
Apoptosis is controlled and does not cause inflammation, whereas necrosis is uncontrolled and triggers inflammation.
125
What happens when apoptosis is reduced?
Cells accumulate, leading to conditions like cancer (neoplasia).
126
What happens when apoptosis is excessive?
Excessive cell loss, leading to conditions like atrophy.
127
What are the main cellular events in apoptosis?
* DNA fragmentation
* Cytoskeletal breakdown
* Mitochondrial dysfunction
* Cell shrinkage
* Formation of apoptotic bodies
128
What nuclear changes occur in apoptosis?
Pyknosis (nuclear shrinkage) followed by karyorrhexis (nuclear fragmentation).
129
How are apoptotic bodies cleared from the body?
They are rapidly phagocytosed by neighbouring cells or immune cells.
130
How is apoptosis regulated?
By an intracellular program involving pro-apoptotic and anti-apoptotic factors.
131
What are two examples of pathological apoptosis?
1. Radiation-induced apoptosis
2. Viral infection-induced apoptosis
132
What are the key differences between necrosis and apoptosis?
* Necrosis: Uncontrolled, inflammatory, involves large groups of cells.
* Apoptosis: Controlled, non-inflammatory, affects individual cells.
133
What happens to cellular contents in necrosis vs. apoptosis?
* Necrosis: Leakage of cell contents.
* Apoptosis: Cellular components are neatly packaged into apoptotic bodies.
134
A patient presents with stroke symptoms. A CT scan shows a cerebral infarction. The patient dies after ten days. What is the most likely type of necrosis seen in the brain?
Liquefactive necrosis.
135
Why does liquefactive necrosis occur in the brain after ischemic injury?
The brain lacks structural proteins that can maintain architecture after cell death, leading to complete tissue digestion.
136
A pathologist examines a lung biopsy from a tuberculosis patient. The tissue appears cheesy and yellow-white. What type of necrosis is this?
Caseous necrosis.
137
A patient with acute pancreatitis has areas of white chalky deposits in their pancreas. What type of necrosis is occurring?
Fat necrosis.
138
What is haemostasis?
A tightly regulated process that keeps blood fluid in normal vessels while allowing clot formation at injury sites.
139
What are the three main components of haemostasis?
1. Vascular wall (endothelium)
2. Platelets
3. Coagulation cascade
140
How is thrombosis different from haemostasis?
Thrombosis is a pathological process where a solid mass of blood components forms inappropriately within the vascular system.
141
What is the main risk of thrombosis in the vascular system?
Thrombi are poorly attached and prone to fragmentation, which can cause embolism.
142
What are the three major factors that contribute to thrombosis?
Virchow’s Triad:
1. Endothelial injury (e.g., trauma, atherosclerosis)
2. Abnormal blood flow (stasis or turbulence)
3. Hypercoagulability (thrombophilia)
143
How does endothelial injury promote thrombosis?
* Exposes the extracellular matrix (ECM)
* Allows platelet adhesion
* Triggers the release of tissue factor, activating the clotting cascade
144
What type of abnormal blood flow is associated with arterial and venous thrombosis?
* Turbulence → Contributes to arterial and cardiac thrombosis
* Stasis → Contributes to venous thrombosis
145
What is hypercoagulability, and what are common causes?
* Increased tendency of blood to clot
* Can be due to genetic factors (e.g., Factor V Leiden mutation) or acquired factors (e.g., prolonged immobility, pregnancy, cancer).
146
Where do arterial thrombi typically form?
At sites of turbulence or endothelial injury, often superimposed on atherosclerosis.
147
What are common sites of arterial thrombosis?
* Coronary arteries (heart attack)
* Cerebral arteries (stroke)
* Femoral arteries (limb ischemia)
148
How do arterial thrombi appear microscopically?
They consist of alternating layers of platelets, fibrin, and red blood cells, known as lines of Zahn.
149
Where does venous thrombosis usually occur?
In superficial or deep veins of the leg (deep vein thrombosis, DVT).
150
Why does venous thrombosis often remain asymptomatic?
Collateral bypass channels can compensate, making about 50% of cases asymptomatic.
151
What are the two main complications of venous thrombosis?
1. Local pain and oedema (due to impaired drainage)
2. Pulmonary embolism (if thrombus dislodges)
152
What is the most common cause of thrombotic lesions in deep veins?
Blood stasis at venous valves, which creates turbulence and promotes clot formation.
153
How can deep vein thrombosis (DVT) be prevented during long flights?
* Leg exercises
* Hydration
* Compression stockings
* Avoiding prolonged immobility
154
What are the four possible outcomes of a thrombus?
1. Propagation – Thrombus enlarges.
2. Embolization – Thrombus dislodges and travels to another site.
3. Dissolution – Thrombus breaks down via fibrinolysis (e.g., t-PA therapy).
4. Organization & recanalization – The thrombus is incorporated into the vessel wall, restoring blood flow.
155
Why are fibrinolytic agents like tissue plasminogen activator (t-PA) most effective when given early?
Because fibrinolysis is most effective within 5 hours of thrombus formation.
156
What are the main complications of arterial thrombosis?
Distal tissue infarction due to obstruction of blood flow.
157
What are the main complications of venous thrombosis?
Congestion, oedema, and embolism due to impaired venous drainage.
158
What is an embolism?
A detached thrombus or fragment that travels through the bloodstream and causes obstruction elsewhere.
159
What happens if a venous thrombus embolizes?
It enters the pulmonary circulation, causing a pulmonary embolism (PE), which can be fatal.
160
What happens if an arterial thrombus embolizes?
It can block downstream organs, leading to stroke, myocardial infarction, or limb ischemia.
161
Why does arterial blood clot formation often occur at sites of atherosclerosis?
Because atherosclerotic plaques cause endothelial injury and turbulent blood flow, promoting clot formation.
162
Why is prolonged bed rest a major risk factor for venous thrombosis?
It causes stasis of blood flow, increasing the likelihood of clot formation.
163
Which type of thrombosis is most commonly associated with heart attacks?
Arterial thrombosis, particularly in the coronary arteries.
164
What is the most effective early treatment for an acute thrombotic event?
Fibrinolytic therapy (e.g., t-PA) to dissolve the clot before permanent damage occurs.
165
All of the following are TRUE about arteries EXCEPT:
(D) Arteries do not have one-way valves (only veins have valves to prevent backflow).
166
What are the five cardinal signs of acute inflammation?
The five cardinal signs of acute inflammation are:
* Rubor (redness)
* Tumor (swelling)
* Calor (heat)
* Dolor (pain)
* Functio laesa (loss of function)
167
Describe the sequence of events in leukocyte recruitment during acute inflammation.
Leukocyte recruitment involves the following steps:
1. Margination and Rolling: Leukocytes move towards the endothelium and roll along its surface, mediated by selectins.
2. Adhesion: Leukocytes firmly adhere to the endothelium, mediated by integrins.
3. Transmigration (Diapedesis): Leukocytes squeeze through the intercellular spaces between endothelial cells.
4. Chemotaxis: Leukocytes migrate towards the site of injury along a chemical gradient, guided by chemoattractants.
168
Explain the process of phagocytosis and the mechanisms involved in killing pathogens.
Phagocytosis involves the following steps:
1. Recognition and attachment: Phagocytes recognize and bind to the pathogen.
2. Engulfment: The pathogen is engulfed by the phagocyte, forming a phagosome.
3. Phagolysosome formation: The phagosome fuses with a lysosome, forming a phagolysosome.
4. Killing and degradation: The pathogen is killed and degraded within the phagolysosome by reactive oxygen species (ROS), reactive nitrogen species (RNS), and lysosomal enzymes.
169
What are the main types of acute inflammatory mediators and their functions?
Acute inflammatory mediators include:
* Vasoactive amines (histamine, serotonin): Vasodilation, increased vascular permeability.
* Arachidonic acid metabolites (prostaglandins, leukotrienes): Vasodilation, pain, fever, leukocyte recruitment.
* Cytokines (TNF-α, IL-1, IL-6): Local and systemic effects, including fever, leukocyte activation, and acute-phase response.
* Chemokines: Leukocyte chemotaxis.
* Complement system: Opsonization, chemotaxis, cell lysis.
170
How does acute inflammation resolve, and what factors can influence the outcome?
Resolution of acute inflammation involves:
* Neutralization and removal of inflammatory mediators.
* Apoptosis of neutrophils.
* Clearance of debris by macrophages.
* Tissue repair and regeneration.
Factors influencing the outcome include:
* Severity and duration of the initial insult.
* Nature of the injurious agent.
* Presence of underlying diseases.
* Effectiveness of the host immune response.
171
What are the potential complications of acute inflammation?
Complications of acute inflammation can include:
* Abscess formation: Collection of pus within a tissue.
* Sepsis: Systemic inflammatory response to infection.
* Chronic inflammation: Persistent inflammation leading to tissue damage and fibrosis.
* Scar formation: Excessive deposition of collagen during tissue repair.
172
How does chronic inflammation differ from acute inflammation?
173
What are the key differences between the two main types of leukocytes involved in acute inflammation: neutrophils and macrophages?
174
Question 10: How can acute inflammation be beneficial to the host?
Acute inflammation is a critical part of the innate immune response and plays a vital role in:
* Eliminating pathogens: Destroying and removing harmful microbes and foreign substances.
* Initiating tissue repair: Promoting healing and regeneration of damaged tissue.
* Preventing further injury: Limiting the spread of infection or damage.
175
What is nomenclature in the context of pathology and medicine?
Nomenclature is the system of names used in pathology and medicine.
176
Why is it important to have a uniform nomenclature for diseases?
Uniform nomenclature helps communication and enables accurate epidemiological studies.
177
What do the suffixes "-itis", "-oma", and "-osis" mean in disease nomenclature? Give an example of each.
* -itis: Indicates an inflammatory process (e.g., appendicitis).
* -oma: Indicates a tumor (e.g., carcinoma).
* -osis: Indicates an abnormal increase (e.g., atherosclerosis).
178
What do the suffixes "-oid", "-plasia", and "-opathy" mean in disease nomenclature? Give an example of each.
* -oid: Means bearing a resemblance to (e.g., rheumatoid disease).
* -plasia: Indicates a disorder of growth (e.g., hyperplasia).
* -opathy: Indicates an abnormal state lacking specific characteristics (e.g., cardiomyopathy).
179
What are eponymous names in the context of disease nomenclature?
Eponymous names are diseases or lesions named after a person or place associated with them (e.g., Graves' disease, Crohn's disease).
180
What are the aims of disease classification?
The aims of disease classification are to:
* Determine the best treatment.
* Estimate the prognosis.
* Ascertain the cause so the disease can be prevented in the future.
181
What is the most widely used basis for disease classification?
The most widely used disease classifications are based on causes (etiology) and underlying mechanisms (pathogenesis).
182
Define and differentiate between genetic, acquired, and congenital diseases.
* Genetic diseases: Caused by abnormalities in the genome. Most are inherited, but ~15-20% occur due to new mutations.
* Acquired diseases: Caused by environmental factors.
* Congenital diseases: Initiated before or during birth. Can be genetic or non-genetic.
183
What are the two main types of congenital diseases? Give an example of each.
* Genetic: Inherited from parents or caused by genetic mutations before birth (e.g., Down's syndrome).
* Non-genetic: Caused by external interference with normal embryonic and fetal development (e.g., deafness and cardiac abnormalities).
184
What are the different classifications of acquired diseases based on pathogenesis?
Acquired diseases can be classified as:
* Inflammatory.
* Haemodynamic.
* Growth disorders.
* Injury and disordered repair.
* Disordered immunity.
* Metabolic and degenerative disorders.
185
What is the definition of "disease"?
A disease is a condition in which the presence of an abnormality in the body causes a loss of normal health. This abnormality can be structural or functional and is due to the inability of the organism to adapt to a challenge. Diseases clinically manifest through signs and symptoms.
186
Explain the two ways in which the terms "primary" and "secondary" are used in disease nomenclature.
1. Causation:
* Primary: Disease without an apparent cause (also called essential, idiopathic, spontaneous, or cryptogenic).
* Secondary: Disease that is a complication or manifestation of some underlying lesion.
2. Stages of a disease: To distinguish between the initial and subsequent stages, most commonly used with cancer.
187
What is the difference between "acute" and "chronic" diseases?
* Acute: Rapid onset, often (but not always) followed by a rapid resolution.
* Chronic: May follow an acute initial episode and has a prolonged course lasting months or years.
188
What is the difference between "benign" and "malignant" tumors?
* Benign tumors: Remain localized to the tissue of origin and are very rarely fatal.
* Malignant tumors: Invade and spread from their origin and are commonly fatal.
189
What does the prefix "ana-" mean in disease nomenclature? Give an example.
"Ana-" means absence or lack of. An example is anaplasia, which refers to a loss of differentiation in cells.
190
What does the prefix "dys-" mean in disease nomenclature? Give an example.
"Dys-" means disordered, difficult, or painful. An example is dysplasia, which refers to abnormal development or growth of cells, tissues, or organs.
191
What does the prefix "hyper-" mean in disease nomenclature? Give an example.
"Hyper-" means excessive or above normal. An example is hypertension, which refers to high blood pressure.
192
What does the prefix "hypo-" mean in disease nomenclature? Give an example.
"Hypo-" means deficient or below normal. An example is hypotension, which refers to low blood pressure.
193
What does the prefix "meta-" mean in disease nomenclature? Give an example.
"Meta-" means change or transformation. An example is metaplasia, which refers to the reversible replacement of one differentiated cell type with another mature differentiated cell type.
194
What does the prefix "neo-" mean in disease nomenclature? Give an example.
"Neo-" means new. An example is neoplasia, which refers to the formation or presence of a new, abnormal growth of tissue.
195
What is meant by the term "pathogenesis"?
Pathogenesis refers to the origin and development of a disease, including the underlying mechanisms and processes involved.
196
What proportion of congenital diseases are estimated to be due to genetic factors?
Approximately 5% of births in the UK have congenital diseases, and of these, a significant proportion are due to genetic factors, either inherited or arising from new mutations.
197
What is the key characteristic of a "chronic" disease?
A chronic disease has a prolonged course, lasting for months or years, and may follow an acute initial episode.
198
What is the difference in fatality between benign and malignant tumors?
Benign tumors are very rarely fatal, while malignant tumors are commonly fatal.
199
What is the difference between a disease and a syndrome?
A disease is a specific condition with a recognizable pattern of signs and symptoms, whereas a syndrome is a collection of signs and symptoms that occur together but may have multiple causes.
200
What is the purpose of using prefixes in disease nomenclature?
Prefixes are used to modify the meaning of root words, providing more specific information about the nature of the disease or condition.
201
Give an example of a disease where the prefix "dys-" is used.
Dysplasia is an example of a disease using the prefix "dys-". It refers to abnormal development or growth of cells, tissues, or organs.
202
What does the prefix "meta-" indicate in the context of disease?
The prefix "meta-" indicates a change or transformation from one state to another. An example is metaplasia, which is the reversible replacement of one differentiated cell type with another mature differentiated cell type.
203
What is the significance of the prefix "neo-" in disease nomenclature?
The prefix "neo-" signifies something new. Neoplasia, for example, refers to the formation or presence of a new, abnormal growth of tissue.
204
Why is it important to distinguish between primary and secondary diseases?
Distinguishing between primary and secondary diseases is crucial for understanding the underlying cause of a condition and determining appropriate treatment strategies.
205
What is an embolus, and how does it differ from a thrombus?
An embolus is a mass (often a fragment of a thrombus) that has broken loose and travels through the bloodstream, potentially lodging in a vessel and blocking it. A thrombus is a blood clot that forms in situ within a blood vessel or the heart.
206
What is the most common source of a pulmonary embolism, and why can it be fatal?
The most common source is a deep vein thrombosis (usually in the legs). If a large embolus lodges in the pulmonary artery (blocking blood flow to the lungs), it can cause sudden death, right heart failure, or cardiovascular collapse.
207
What are some other possible types of emboli besides thromboembolism?
Besides fragments of thrombus, emboli can be from:
* Infected lesions (septic emboli)
* Gas bubbles (air or nitrogen in divers who ascend too quickly)
* Fat or bone marrow (from fractures)
* Tumor cells (metastatic spread)
* Amniotic fluid (rarely, during labor)
208
What determines the outcome of an embolus once it enters the circulation?
The outcome depends on:
1. Where it originates (venous vs arterial system)
2. Where it lodges (lung, brain, kidney, limbs, etc.)
3. Blood flow and presence of collateral circulation in that tissue
209
What is a systemic (arterial) embolus, and where does it often come from?
A systemic arterial embolus travels in the arterial circulation (rather than veins). About 80% arise from inside the heart (e.g., from mural thrombi in the left ventricle after a myocardial infarction). These emboli can lodge in major organs (brain, kidneys, spleen, etc.), causing infarction.
210
Define “infarction.”
Infarction is an area of ischemic necrosis within a tissue/organ due to occlusion of its arterial supply or venous drainage. Most are caused by thrombotic or embolic events leading to hypoxia and cell/tissue death.
211
What are some non-thrombotic causes of infarction?
Though most infarcts stem from thrombotic or embolic occlusions, other causes include:
* Vasospasm (sudden vessel spasm)
* Hemorrhage into an atherosclerotic plaque
* External compression (e.g., by a tumor)
* Traumatic rupture of a vessel
212
How are infarcts classified by color, and what does each type imply?
1. White (anemic) infarcts: Occur in solid organs (e.g., heart, kidney, spleen) with end-arterial circulation.
2. Red (hemorrhagic) infarcts: Typically found in tissues like the lung or in organs with dual blood supply or venous occlusion.
3. Septic vs. bland infarcts: Depends on whether infection is present.
213
Which major factors influence the outcome of an infarction in a particular tissue?
1. Nature of the vascular supply (availability of alternate blood routes)
2. Rate of occlusion (sudden vs. gradual)
3. Tissue vulnerability to hypoxia (neurons and myocardial cells are very sensitive)
4. Oxygen content of the blood (e.g., anemia worsens infarction)
214
In myocardial infarction, why can gross changes be difficult to see in the first few hours?
Early after coronary occlusion (2–6 hours), gross morphological changes in heart muscle are not yet visible. Visible or microscopic changes typically appear 24+ hours post-occlusion.
215
Summarize “shock” in medical terms.
Shock is best described as inadequate tissue perfusion due to systemic hypotension, which arises from reduced cardiac output or insufficient circulating blood volume. It results in diminished oxygen/nutrient delivery to tissues and can lead to organ failure and death if untreated.
216
What are the main categories (causes) of shock?
1. Cardiogenic shock: Heart failure (e.g., myocardial infarction) → low cardiac output
2. Hypovolemic shock: Reduced blood/plasma volume (e.g., hemorrhage, severe burns, diarrhea) → decreased preload and output
3. Septic shock: Intense vasodilation and peripheral pooling (often due to systemic infection/toxins) → reduced effective circulating volume
217
What are common signs/symptoms indicating a person may be in shock?
* Rapid, weak pulse and low blood pressure
* Cool, pale, or bluish skin (poor perfusion)
* Confusion or altered mental status
* Rapid breathing
* Nausea/vomiting
* Excessive thirst
* Cold, clammy extremities
218
What first-aid steps can be taken if someone appears to be in shock?
1. Lay the person down and elevate the legs (to improve venous return).
2. Keep the person warm (cover with a blanket).
3. If no neck injury is suspected, turn the head to one side to prevent airway obstruction from possible vomiting.
4. Call emergency services promptly; severe shock is life-threatening.
219
Why can severe blood or fluid loss (e.g., from hemorrhage or burns) lead to hypovolemic shock?
The effective circulating blood volume drops too low, reducing venous return to the heart. This leads to decreased cardiac output and systemic hypotension, diminishing tissue perfusion.
220
How does septic shock cause dangerously low blood pressure?
During sepsis or severe infection, inflammatory mediators cause widespread vasodilation and increase vascular permeability. Blood pools in expanded peripheral vessels, and the effective circulating volume plummets, leading to hypotension and inadequate perfusion.
221
Why is shock considered a “final common pathway” of many lethal events?
Various acute conditions (e.g., massive bleeding, severe heart failure, overwhelming infection) can converge on systemic hypotension and inadequate tissue perfusion. Untreated shock rapidly leads to organ dysfunction, multi-organ failure, and death.
222
Approximately how many liters of blood does an average 70-kg adult male have?
About 5 liters of blood. Losing over a third of this volume quickly (e.g., hemorrhage) can induce life-threatening shock.
223
What is the general definition of inflammation, and why is it considered fundamentally protective?
Inflammation is the biological response to noxious or harmful stimuli (e.g., microbes, burns, trauma). It’s fundamentally protective because it aims to eliminate the cause of injury or infection, remove damaged cells, and initiate tissue repair, although it can also lead to tissue damage if excessive.
224
What are the four classical signs of acute inflammation originally described by Celsus?
1. Rubor (Redness)
2. Tumor (Swelling)
3. Calor (Heat)
4. Dolor (Pain)
Virchow later added Functio Laesa (Loss of function) as a possible fifth sign.
225
How does “acute” inflammation differ in timing from “chronic” inflammation?
Acute inflammation is a rapid response that typically begins immediately (minutes to hours) and lasts hours to a few days. Chronic inflammation persists much longer (weeks to months or even years).
226
What main goals does the body aim to accomplish during acute inflammation?
To increase blood flow to the site of injury (bringing leukocytes, antibodies, etc.), increase vascular permeability (letting fluid/proteins/cells exit circulation), and recruit and activate leukocytes to eliminate offending agents or debris.
227
Which types of stimuli commonly trigger acute inflammation?
Infections (bacterial, viral, fungal, parasitic)
* Trauma (blunt or penetrating)
* Burns/frostbite (thermal, chemical)
* Allergic reactions
* Tissue necrosis (e.g., infarction, hypoxia)
228
Name the three major components (steps) of acute inflammation.
1. Vascular dilation → increases blood flow.
2. Microvascular structural changes → plasma proteins and leukocytes leave circulation.
3. Emigration of leukocytes → cells accumulate at the injury site and activate to clear the offending agent.
229
Which mediators are primarily responsible for vasodilation in acute inflammation, and what clinical signs do they produce?
Histamine, bradykinin, and nitric oxide (NO) mediate vasodilation. They cause redness (rubor) and heat (calor) by increasing local blood flow (hyperemia).
230
Why does vascular permeability increase during acute inflammation, and what does this cause?
The endothelium becomes leaky due to endothelial cell contraction, injury, or (less commonly) transcellular transport. This leakage lets plasma fluid and proteins exit into the tissues, causing edema (the swelling or tumor).
231
Describe how leukocytes exit the bloodstream and reach the site of tissue injury (extravasation).
1. Margination & rolling (mediated by selectins on endothelium).
2. Firm adhesion (via integrins like ICAM-1, VCAM-1).
3. Transmigration (diapedesis) across the endothelium.
4. Chemotaxis through tissue along a gradient of chemoattractants until they reach the injury site.
232
What is “chemotaxis,” and which substances commonly act as chemoattractants?
Chemotaxis is the directed migration of leukocytes toward the injury site guided by chemical gradients. Common chemoattractants include:
* Bacterial products
* Complement components (e.g., C5a)
* Cytokines (e.g., IL-8)
* Leukotriene B4
233
Which leukocytes typically predominate early in acute inflammation, and what is their main function?
Neutrophils usually predominate initially. They phagocytose microbes and cellular debris, release granule enzymes, and generate reactive oxygen species to kill pathogens.
234
What are “phagolysosomes,” and why are they critical for pathogen destruction?
When a leukocyte engulfs a microbe, it forms a phagosome that later fuses with a lysosome. This phagolysosome contains digestive enzymes and often reactive oxygen species that degrade or kill the ingested pathogen.
235
Name three important pro-inflammatory cytokines and their general effect in acute inflammation.
1. TNF-α
2. IL-1
3. IL-6
They amplify the inflammatory response, promote endothelial activation, and help recruit/activate other immune cells.
236
How can acute inflammation be morphologically classified (patterns)?
1. Serous (thin fluid; e.g., skin blister)
2. Fibrinous (fibrin-rich exudate)
3. Purulent (pus; e.g., abscess)
4. Ulcerative (necrotic tissue loss at surface)
237
Define what “purulent inflammation” is and give an example.
Purulent inflammation is characterized by pus—a thick fluid of neutrophils, necrotic cells, and fluid exudate. An example is abscess formation, often due to Staphylococcus infections.
238
What are the possible outcomes of acute inflammation?
1. Complete resolution (restoration to normal)
2. Healing by connective tissue/fibrosis (scar formation)
3. Progression to chronic inflammation if the injurious agent persists or if the response is dysregulated
239
Under what conditions does acute inflammation typically resolve completely rather than progress to fibrosis?
When the injury is mild, short-lived, and limited in scope, with minimal tissue damage and the ability for regeneration. Effective elimination of the cause and efficient removal of exudate/debris also favor resolution.
240
Why might extensive acute inflammation lead to scarring (fibrosis)?
If there is substantial tissue damage, or if the tissue cannot regenerate (e.g., destructive infection or severe necrosis), fibroblasts proliferate, depositing collagen and forming a scar that replaces the functional tissue.
241
In an MCQ context, a question states: “Acute inflammation is a rapid host reaction in response to which of the following situations?” and lists infections, trauma, burns, allergy, or “all of the above.” What is the best answer?
All of the above. Acute inflammation can be triggered by infections, trauma (mechanical injury), burns/frostbite, and allergic reactions—among other causes.
242
What fundamentally distinguishes chronic inflammation from acute inflammation in terms of duration and clinical signs?
Chronic inflammation typically persists for months or years, sometimes lifelong, and often lacks the four or five classical acute signs (rubor, tumor, calor, dolor, functio laesa). Acute inflammation lasts hours to days and usually shows those classical signs (e.g., redness, swelling).
243
Under what circumstances can chronic inflammation develop?
1. Progression from unresolved or recurrent acute inflammation. 2. De novo onset (no preceding acute phase), e.g., certain autoimmune or granulomatous conditions.
244
List the three main categories of causes of chronic inflammation.
1. Persistent infection (organisms difficult to eliminate, e.g., Mycobacterium tuberculosis) 2. Immune-mediated inflammatory diseases (autoimmune, allergic, e.g., rheumatoid arthritis, asthma) 3. Prolonged exposure to toxic agents (exogenous like asbestos or endogenous accumulations)
245
Why is chronic inflammation relevant to many prevalent diseases in modern society?
It underlies or contributes to many chronic conditions (e.g., atherosclerosis, autoimmune diseases, neurodegenerative diseases, certain lung pathologies, and cancer), making it a major driver of morbidity and mortality.
246
What are the hallmark morphological features of chronic inflammation?
1. Infiltration with mononuclear cells (macrophages, lymphocytes, plasma cells). 2. Tissue destruction (often progressive). 3. Attempts at healing (angiogenesis + fibrosis) occurring simultaneously with ongoing inflammation.
247
Which cell types typically dominate in chronic inflammation, and how do they contribute?
Macrophages: Key effector cells, secrete cytokines causing further tissue damage/fibrosis, and can form granulomas. Lymphocytes: T-cells produce cytokines (e.g., IFN-γ) activating macrophages; B-cells → plasma cells → antibodies. Plasma cells: Derived from activated B-cells, secrete specific antibodies. Eosinophils/Mast cells: Often present in parasitic infections or allergies.
248
What role do macrophages play in chronic inflammation, and how do they interact with lymphocytes?
Macrophages ingest pathogens or debris, present antigens to T-cells, and secrete cytokines. In turn, T-lymphocytes secrete IFN-γ to further activate macrophages, creating a positive feedback loop that perpetuates chronic inflammation.
249
Define a granuloma and mention two distinct types.
A granuloma is a specialized form of chronic inflammation where activated macrophages (epithelioid cells) and sometimes giant cells aggregate around a difficult-to-remove agent. Two types are: 1. Caseating (e.g., tuberculosis) 2. Non-caseating (e.g., sarcoidosis)
250
What is the usual pathophysiological reason for granuloma formation?
Granulomas form when the offending agent (microbe, foreign material) cannot be effectively cleared by normal phagocytosis. The immune system walls it off with aggregates of macrophages, giant cells, and lymphocytes.
251
How can chronic inflammation harm host tissues even though it aims to contain the offending agent?
Prolonged inflammation leads to ongoing tissue necrosis, fibrosis, and potentially loss of organ function. Macrophage and lymphocyte products (ROS, cytokines) can damage healthy cells.
252
Name some systemic effects (whole-body manifestations) of chronic inflammation.
1. Fever (low-grade, persistent) 2. Elevated acute-phase proteins (C-reactive protein, fibrinogen, SAA) 3. Leukocytosis (raised white cell count) 4. Mild anemia, weight loss, increased pulse/BP, and general malaise.
253
Why does fever occur in chronic inflammation?
Cytokines (e.g., IL-1, TNF) alter the thermostatic set point in the hypothalamus, causing the body to increase heat production (via shivering, decreased sweating) and reduce heat loss, resulting in fever.
254
Which lab findings often increase during chronic inflammation, useful as clinical markers?
CRP (C-reactive protein) Fibrinogen Serum amyloid A (SAA) White blood cell count (especially in bacterial infections)
255
What are the final outcomes of chronic inflammation if it is not resolved?
Fibrosis (scar formation) Potential loss of organ function Continual or escalating tissue damage (In some cases) predisposition to neoplastic changes
256
In comparing acute vs. chronic inflammation, how do they differ in vascular changes, cellular infiltration, and tissue repair sequence?
Acute: Rapid onset, neutrophils predominate, marked vascular changes (edema, redness), repair begins after inflammation ends. Chronic: Persistent, macrophages/lymphocytes predominate, fewer visible vascular changes (no marked edema), ongoing repair (fibrosis, angiogenesis) concurrently with inflammation.
257
Provide an example of a pathological condition that features granulomatous chronic inflammation.
Tuberculosis (Mycobacterium tuberculosis infection) is a classic cause, featuring caseating granulomas with Langerhans giant cells.
258
In an MCQ context, matching “Plasma cells” with “phagocytosis” is correct or incorrect?
Incorrect. Plasma cells secrete antibodies; phagocytosis is performed by macrophages and neutrophils, not plasma cells.
259
What does “cellular adaptation” mean in the context of pathology?
Cellular adaptation refers to the ways cells adjust their structure and function in response to increased or decreased demands or stress, often to avoid injury or keep functioning.
260
Under what circumstances does a cell typically undergo hypertrophy vs. hyperplasia?
Hypertrophy: When cells increase in size, due to synthesis of more structural components (often seen in tissues with limited cell division, e.g., muscle). Hyperplasia: When cells increase in number via cell division (e.g., epithelial or glandular tissues).
261
Define hyperplasia, and how does it differ from cancerous growth?
Hyperplasia: A controlled increase in the number of cells, leading to tissue/organ enlargement. Cancerous growth: An uncontrolled proliferation that does not respond to normal regulatory signals.
262
What are the main molecular mechanisms that can trigger hyperplasia?
1. Increased local production of growth factors. 2. Increased expression of growth factor receptors on cells. 3. Enhanced intracellular signalling pathways that lead to gene transcription and cell proliferation.
263
What is hypertrophy, and what are common examples of physiological vs. pathological hypertrophy?
Hypertrophy: Increase in cell size (and thus organ size) due to increased synthesis of structural proteins. Physiological example: Skeletal muscle hypertrophy from exercise. Pathological example: Cardiac hypertrophy in response to hypertension or valve disease.
264
Summarize the two main biochemical pathways leading to muscle hypertrophy.
1. Physiological: IGF-1 → PI3K → Akt pathway (e.g., muscle growth from exercise). 2. Pathological: Ang II, ET-1, or NA → G-protein-coupled receptors (Gαq/11) → MAPK/PKC/PKA → excessive or maladaptive hypertrophy (e.g., heart under high blood pressure).
265
Differentiate hyperplasia from hypertrophy with a simple example.
Hyperplasia: Four cells → eight cells (cell number doubles, same size). Hypertrophy: Four cells → four enlarged cells (cell size increases, number unchanged).
266
What is atrophy, and why can it be considered an adaptive process?
Atrophy is the shrinkage (reduced size) of a tissue or organ due to decreased cell size and number. It’s adaptive because it helps cells/tissues minimize energy demands or resources if stimuli (e.g., blood flow, nutrition) are reduced.
267
List some common causes of atrophy.
1. Decreased workload (disuse) 2. Loss of innervation (denervation) 3. Diminished blood supply (ischemia) 4. Inadequate nutrition 5. Loss of endocrine stimulation 6. Pressure (compression)
268
What is metaplasia, and when might it occur?
Metaplasia is when one mature cell type changes to another mature cell type better able to endure new conditions (e.g., respiratory epithelium changing to squamous in a smoker’s airways).
269
Define “healing responses” after injury and how regeneration differs from scar formation.
Healing is the body’s way of restoring tissue integrity post-injury. Regeneration fully replaces damaged cells with original cell types, preserving function. Scar formation (fibrosis) uses collagen and fibrous tissue to patch damage, potentially losing normal function.
270
What factors determine whether healing occurs primarily by regeneration or by fibrosis (scar formation)?
1. Tissue’s intrinsic ability to regenerate (e.g., labile vs. stable vs. permanent cells). 2. Extent of the injury (smaller or superficial injuries more likely to regenerate; extensive damage often leads to scarring).
271
Give examples of tissues that exhibit continuous (labile), stable, and permanent cell turnover.
Labile (continuous): Skin epidermis, GI tract epithelium, hematopoietic cells. Stable: Liver, kidney tubule cells (can regenerate if needed). Permanent: Neurons, cardiac muscle (minimal to no regenerative capacity).
272
Why is stem cell function crucial for tissue regeneration?
Stem cells can self-renew and differentiate into needed mature cells, making them vital for replacing lost or damaged cells in regenerative tissues (e.g., skin, gut lining, bone marrow).
273
Compare embryonic stem cells (ES) with adult (somatic) stem cells.
ES cells: Pluripotent, can form all tissue types; found in the inner cell mass of blastocysts. Adult stem cells: Typically multipotent or more lineage-restricted, reside in specific niches (e.g., bone marrow, basal layer of skin).
274
What are induced pluripotent stem cells (iPSCs), and why might they overcome some ethical or rejection issues?
iPSCs are adult somatic cells (e.g., skin fibroblasts) genetically reprogrammed to pluripotent status. Because they originate from the patient’s own cells, they sidestep many immune rejection and ethical problems associated with embryonic stem cells.
275
What is the main safety concern in using stem cells for regenerative therapy?
Their intrinsic capacity for rapid proliferation and self-renewal can, if dysregulated, lead to tumorigenesis (i.e., formation of teratomas or other malignancies).
276
Why is understanding stem cell biology important for advancing medical research and therapy?
1. Elucidates developmental signals and differentiation steps. 2. Aids in creating knockout models for disease study. 3. Enables potential regeneration of damaged organs (e.g., cell-based transplant therapies).
277
What is 'growth' in the context of tissue biology?
Growth is the process by which a tissue increases in size through the synthesis of specific cellular components.
278
How is 'differentiation' defined?
Differentiation is the process by which a cell develops a specialized function or morphology that distinguishes it from its parent cells.
279
What does 'tumour differentiation' refer to?
It refers to the extent to which neoplastic cells resemble the normal cells of the tissue from which they arise, both morphologically and functionally.
280
Define 'anaplasia.'
Anaplasia is the loss of cellular differentiation—a reversion from a highly differentiated state to a less specialized, primitive state—and is a hallmark of malignant transformation.
281
Name one morphological change seen in anaplastic cells.
Pleomorphism, which is marked variation in cell size and shape.
282
Give another example of a change associated with anaplasia.
Abnormally large nuclei that contain an abundance of DNA relative to the cell size.
283
What is 'neoplasia'?
Neoplasia is the process of new, uncontrolled cell growth that forms a neoplasm or tumour, which grows uncoordinated with normal tissues.
284
How is a tumour defined?
A tumour is an abnormal mass of tissue resulting from neoplasia, where the growth exceeds and is uncoordinated with that of the normal tissue, persisting even after the original stimulus ceases.
285
What distinguishes a benign tumour from a malignant tumour?
Benign tumours are non-invasive, remain localized, have a slow growth rate, and are often encapsulated, whereas malignant tumours are invasive, can metastasize, grow rapidly, and exhibit disordered cellular architecture.
286
How are benign epithelial tumours commonly named?
They are typically called papillomas or adenomas.
287
How are malignant epithelial tumours named?
Malignant epithelial tumours are called carcinomas.
288
What term is used for malignant connective tissue tumours?
They are known as sarcomas.
289
What does the suffix '-oma' indicate in tumour nomenclature?
It is used to denote a neoplasm or tumour, whether benign or malignant, though additional descriptors clarify behavior (e.g., carcinoma, sarcoma).
290
Define metaplasia.
Metaplasia is a reversible change in which one differentiated adult cell type is replaced by another that is better able to withstand adverse conditions.
291
Why is metaplasia clinically important?
Although adaptive, persistent metaplasia may predispose tissue to dysplasia and subsequent malignant transformation.
292
What is dysplasia?
Dysplasia is disordered growth where cells lose uniformity and proper orientation; it is often a pre-neoplastic lesion seen especially in metaplastic epithelia.
293
List one characteristic of dysplastic cells.
They exhibit considerable pleomorphism with variable cell shapes and sizes.
294
What is a hyperchromatic nucleus?
A nucleus that stains more darkly due to an increased DNA content, often seen in dysplastic or malignant cells.
295
What does 'metastasis' mean?
Metastasis is the process by which tumour cells spread from the primary site to distant locations, forming secondary tumour implants.
296
Name one common route of metastatic spread.
Lymphatic spread, where tumour cells travel through lymphatic vessels to regional lymph nodes.
297
What is another pathway for metastasis?
Haematogenous spread, in which tumour cells enter the bloodstream and form metastases in distant organs.
298
What does 'direct seeding' refer to in metastasis?
Direct seeding is the spread of tumour cells across body cavities or surfaces (e.g., pleural, pericardial, or peritoneal cavities).
299
What are oncogenes?
Oncogenes are mutated forms of normal growth-promoting genes that drive uncontrolled cell proliferation.
300
What is the function of tumour suppressor genes?
Tumour suppressor genes normally inhibit cell proliferation; their inactivation removes these growth restraints, contributing to carcinogenesis.
301
What role do apoptosis-regulating genes play in cancer?
They control programmed cell death, and when altered, they can allow damaged cells to survive and proliferate.
302
What are DNA repair genes?
DNA repair genes are responsible for correcting genetic errors; defects in these genes lead to accumulation of mutations that can drive carcinogenesis.
303
Define hyperplasia.
Hyperplasia is an increase in the number of cells within a tissue, resulting in tissue enlargement.
304
What is hypertrophy?
Hypertrophy is the increase in the size of individual cells, leading to an increase in tissue mass.
305
What does atrophy refer to?
Atrophy is the reduction in cell size or number, resulting in the shrinkage of a tissue.
306
How do benign tumours differ from malignant tumours regarding local invasion?
Benign tumours are non-invasive and remain localized, while malignant tumours invade surrounding tissues and can metastasize.
307
What is the significance of a fibrous capsule in benign tumours?
A fibrous capsule helps separate benign tumours from the surrounding tissue, making them well-circumscribed and often easier to remove surgically.
308
Which of the following is not used in cancer therapy: surgical removal, radiotherapy, chemotherapy, growth hormone therapy, or immunotherapy?
Growth hormone therapy is not used as a treatment for cancer.
309
What does the term 'neoplasia' literally mean?
Neoplasia literally means 'new growth,' referring to the abnormal, unregulated proliferation of cells.
310
What is meant by tumour 'differentiation'?
Tumour differentiation describes how much tumour cells resemble their normal counterparts; well-differentiated tumours closely mimic normal tissue, whereas poorly differentiated tumours do not.
311
What is pleomorphism, and in which context is it used?
Pleomorphism is the variation in size and shape among cells, and it is a common feature seen in anaplastic and malignant cells.
312
What are tumour giant cells?
Tumour giant cells are unusually large cells, often formed by the fusion of several cells, and are characteristic of anaplastic or highly malignant tumours.
313
Why is dysplasia considered a pre-neoplastic condition?
Dysplasia involves disordered growth and architectural disturbance; if persistent, it can progress to carcinoma in situ and eventually to invasive cancer.
314
What does metastasis indicate about a tumour?
Metastasis indicates that a tumour is malignant since only malignant tumours have the capacity to spread to distant sites.
315
How does lymphatic spread contribute to metastasis?
Tumour cells enter lymphatic vessels and travel to regional lymph nodes, where they may establish secondary tumour sites.
316
How does haematogenous spread differ from lymphatic spread?
In haematogenous spread, tumour cells enter the bloodstream and can form metastases in distant organs, such as the liver or lungs.
