7.1, 7.2, 8.1 Neoplasia I, II, General pathology of infectious disease

7.1 Neoplasia I
1. Tumours, neoplasms, components
1. Tumour – Abnormal swelling
2. Neoplasm – Lesion resulting from abnormal growth of cells even when stimulus absent
Components of tumours & neoplasms – neoplastic cells + Stroma (CT framework that provides support & nutrition to neoplastic cells)
2. Characteristics – Benign & malignant
1. Slow growth, rapid growth
2. Resembles normal tissue, Poor resemblance
3. Non-invasive, invasive
4. Never metastasises, Frequent metastases
5. Rare ulceration/necrosis, Frequent ulceration/necrosis
3. Clinical effects of benign & malignant
1. Pressure on adjacent tissues, pressure on adjacent tissues
2. Obstruction of flow, obstruction of flow
3. Production of hormone, production of hormone
4. Anxiety, anxiety & pain
5. Transformation into malignancy – Cancer cachexia (weight loss), Metastases
4. Names of Benign & malignant
Benign – Papilloma, Adenoma + Chondroma, Fibroma, Cystadenoma
Malignant – Carcinoma (epithelium), sarcoma (mesenchyme), Adenocarcinoma (gland/duct) + Melanoma, Lymphoma, Mesothelioma, Seminoma
5. Differentiation, Anaplasia Dysplasia
1. Differentiation – Extent to which neoplasms result parent cells
2. Anaplasia – Lack of differentiation -> sign of malignancy
3. Dysplasia – Loss of cell uniformity & architecture (“pre-malignancy)
6. Dysplasia in oral epithelium
1. Loss of uniformity – Variation in cell size/shape | Abnormal mitotic figures
2. Loss of architecture – Increased number of mitotic figures | Superficial mitotic figures | Loss of epithelial cell adhesion
7. Classes of carcinogens
1. Chemicals – Tobacco smoke, aromatic hydrocarbons
2. Viruses – HPV, epstein barr, Hep B&C
3. Radiation
4. Exogenous hormones
5. Microbes
8. Host factors in carcinogenesis
1. Race
2. Diet
3. Constitutional factors (sex/age/race)
4. Premalignant lesions
5. Transplacental exposure
9. 6 Major pathogens in odontogenic infections
1. Strep milleri
2. Peptostreptococcus
3. Other anaerobic streptococci
4. Prevotella species
5. Porphyromonas species
6. Fusobacterium species

7.2 Neoplasia II
1. Hallmarks of cancer
1. Self-sufficiency in growth signals – Gain in function of CDK-4& cylin-D (more cell proliferation) + Loss of function in CDKI (less inhibition of cell proliferation)
2. Insensitivity to growth-inhibiting signals – Mutation in one of the key cell regulators (p16, RB, CDK4, cyclin D). p53 also often mutated
3. Altered cell metabolism – High glucose uptake & fermentation
4. Evasion of cell death – Cancer cells overexpress anti-apoptotic genes (BCL-2, BCL-XL)
5. Unlimited replicative potential – Cancer cells reactivate telomerase
6. Sustained angiogenesis
7. Invasion & metastases
8. Evasion of immune surveillance
2. Enabling characteristics of malignancy
1. Genomic instability + 2. Tumour-promoting inflammation
3. Mechanisms of viral carcinogenesis
1. Oncogenic DNA virus
2. Acute-transforming RNA retrovirus
3. Slow-transforming oncogene
4. Genetic abnormalities in tumours
Tumour suppressor genes
1. 2-hit hypothesis – 1. Inheritence of defective allele of tumour-suppressor gene + 2. Acquired mutation loss of function of normal allele
2. Caretaker genes – repair DNA damage, Gatekeeper genes – Promote death of cells with damaged DNA (e.g. p53, RB)
-Oncogenes – genes that drive the neoplastic behaviour of cells
1. 5 groups of oncogenes
1. Growth factors
2. Growth factor receptors
3. Signalling mediator with tyrosine kinase activity
4. Signalling mediator with nucleotide binding activity
5. Nuclear binding transcription
Detection of oncogene expression
1. Presence of more oncoprotein
2. Increased mRNA transcripts of oncogene
3. Increased copies of oncogene in genome
Oncogenes activated by
1. Mutation
2. Overproduction of oncoprotein
-Epigenetic contribution to tumours
1. Gene silencing
2. Gene up/downregulation from histone modification
3. Interference with gene transcription by microRNA
4. Copy number changes

8.1 General pathology of infectious disease
0. Mechanisms of microbial pathogenesis
1. Enter/contact host cell = death of infected cell
2. Toxins = Kill cells or produce enzymes that degrade components
3. Induce host immune response = Further tissue damage
1. Prions
-Abnormal form of host protein
-Disease occurs when PrP undergoes conformational change that confers resistance to proteases
e.g. Kuru, Creutzfeld-Jakob, BSE
2. Viruses
-Can cause transient illness – influence
-Can cause chronic persistent illness – Hep B
-Can cause neoplastic transformation e.g. HPV
Determinants of viral effects/tropism influenced by
1. Host receptors for viruses
2. Specificity of transcription factors
3. Physical characteristics of tissues
Mechanisms of viral injury
1. Direct cytopathic effects
2. Anti-viral immune response
3. Transformation of infected cells
3. Bacteria
Mechanisms of bacterial injury
1. Adherence – Adhesins help bacteria adhere to cell e.g. Pili on N. gonorrhoea
2. Invasion
3. Toxin production (Endotoxin – An LPS that is a component of the outer bacterial membrane
(Exotoxin – secreted product that causes damage e.g. Enzymes, A-B toxins, Secreted proteins)
Bacteria can also take forms that increase virulence
1. Bacteriophage/plasmids
2. Biofilm
3. Quorum sensing
4. Fungi
-Superficial/deep infections
-Opportunistic/endemic species
5. Protozoa
-Single celled eukaryotes
1. Entamoeba histiolytica in contaminated food/water
2. Bloodborne protozoa by insects e.g. Leishmania
3. Uncooked meat w/ cysts e.g. Toxoplasma gondii
6. Helminths
1. Parasitic worms
1. Round worms
2. Tapeworms
3. Fluke
7. Ectoparasites
-Insects e.g. Fleas
-Arachnids e.g. ticks
8. Routes of microbial entry
1. Skin break (HIV needle stick
2. Inhalation – Influenza virus
3. Ingestion – Salmonella
4. Sexual transmission – HPV
9. Transmission of microbes
1. Horizontal transmission (between unconnected people)
Skin, Oral secretions, Respiratory secretions, blood, urine
2. Vertical transmission (between mother & baby via breastfeeding or pre childbirth)
10. Evasion of microbes
1. Antigenic variation
2. Modification of surface proteins
3. Overcoming antibodies & complement
4. Resist phagocytosis
5. Decreased T-cell recognition
11. Harmful effects of host immune response
1. Granulomatous inflammation
2. T-cell mediated inflammation
3. Innate immune inflammation
4. Humoral immunity
5. Chronic inflammatory disease
6. Cancer
12. Inflammatory responses to infection
1. Suppuration
2. Mononuclear/granulomatous
3. Cytopathic
4. Necrosis
5. Chronic inflammation/scarring

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