Pathology + Tumours Flashcards

1
Q

Features of viral pathogenesis

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2
Q

What is pathogen and commensal

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3
Q

What does colonisation mean

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4
Q

Latent or asymptomatic infection

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5
Q

Features of clinical infection

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6
Q

Pathogenicity

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7
Q

Concepts of infectivity and virulence

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8
Q

Features of pathogenic toxins and their effects

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9
Q

Sites of viral entry

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10
Q

Features of acute viral infections with examples

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11
Q

Features of enterovirus infection and examples

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12
Q

How virus can induce tumours with examples

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13
Q

Humoral and cell mediated immunity

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14
Q

How allergens induce immediate immune response during early phase allergy

A

IgE mediates effects
Activate mast cells

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15
Q

Relationship between (IgE and IgG) and Fc receptors

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16
Q

What is atopy

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Predisposition to allergy

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17
Q

Differences between type 2 and 3 antibody mediated hypersensitivity

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18
Q

Factors mediated by T cells cause tissue damage and autoimmune disease

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19
Q

Contrast systemic and organ specific autoimmune disease

20
Q

What does the ectoderm consist of

A
  • skin
    -nerves
    -melanocytes
21
Q

What does the mesoderm consist of

A

Muscle
Blood
Bone
Cartilage
Endothelium
Serous membrane

22
Q

What does the endoderm consist of

A

Lining of airways
Lining of gut
Glands

23
Q

Hyperplasia

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Beyond formation
( ells increase in number)

24
Q

Hypertrophy

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Beyond nourishment
(Cells become larger in size)

25
Atrophy
Without nourishment (Cells decrease in size)
26
Metaplasia
Change in formation (Make cell change e.g. columnar epithelium to squamous metaplasia)
27
Tumor
Swelling
28
Neoplasia
New formation (Abnormal growth of tissue, uncoordinated proliferation,, can result in cessation of stimuli)
29
Benign vs malignant
Benign: well born, neoplasm does not invade or metastasise (move away from primary location)
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Cancer
Non-specific/non-technical term for a malignant neoplasm
31
Carcinoma
Epithelium
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Sarcoma Leukaemia Lymphoma Others
Connective tissue White blood cells in blood Lymphoid cells
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Physical properties of cancer cells
Pleomorphic (alter shape and size in response to environmental factors) Hyper chromatic (Stain more deeply that normal) Coarse chromatin ((irregular clumps varying in shape and size) Highly mitosis and abnormal forms Disorganised structure
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Behaviour of normal cells
Replicate when required Stick together and replicate when required Specialised to specific role Die when instructed
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Behaviour of cancer cells
Unregulated growth Loss of cohesion Immaturity Immorality
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Carcinogenesis
Tumour angiogenesis: required to sustain growth, escape route Apoptosis: programmed cell death, active process Necrosis: premature cell death, passive process
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What is an oncogene, protooncogene and tumour suppressor
Oncogene: gene with potential to cause cancer Pro-oncogene: helps cells stay alive, helps cells grow and divide to form new cells Tumour suppressor: inhibit cell proliferation,
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How does cancer spread
Metasis: -multiple step process -extracellular matrix remodelling -loss of cell-to-cell and cell-to-matrix adhesion
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Lymphatic spread of cancer
-invade connective tissue -enter lymphatic -travel through lymphatics -exit lymphatics -enter lymph node -grow in lymph node
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Trans-coelomic spread of cancer
Spread through body cavity -peritoneal: gastric, colonic, ovarian -pleural: lung
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Local effects of cancer
- Brain: confusion, coma, seizure - colon: haemmarshage, constipation, diarrhoea - bone: pain, anaemia, fracture - lung: haemoptysis, dyspnoea - spine: paraethesia, paralysis - liver: jaundice, coagulopathy - side effects: immunosuppression, fatigue, hair loss
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Systemic effects of cancer
- Cachexia: weakness, wasting due to chronic illness, muscle/fat loss - paraneoplastic syndromes: tumours abnormally or inappropriately produce hormones (ACTH, PTH, adh) -
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Dysplasia and intra-epithelia neoplasia
- Dysplasia: disorder of cell growth, does not invade
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Key processes and genes in cell cycle
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Environmental vs inherited factors in carcinogenesis
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Multi step nature of carcinognesis